Advertisement

Have you ever wondered, what is your physiological age? Is it more or less than your chronological age? Physiological age determines a person’s health condition. Are we able to determine physiological age? You would think the answer is NO. but it can be done by determining telomere’s length. “Telomere is a repetitive nucleotide sequence (having no meaningful information) at each end of chromosome to protect DNA from deterioration and or from fusion with other chromosomes.” This sequence is about 3000-15000 base pairs in length. In vertebrates this repeated sequence is TTAGGG.
 
Significance of Telomeres
 
Cells divide and increase their number, DNA duplication also occurs. Enzymes involved in this duplication process, can’t continue duplication all the way to the end so some part of DNA is lost and chromosome is shortened. This lost part is some base pairs of telomere. Somatic cells lose about 50-100 nucleotides on each cell division. In this way, telomeres, having no meaningful information, act as CAPS preventing the important information (DNA) from deterioration and preserve the critical information. Telomeres are never tied to each other which allows chromosomes to remain segregate. Without telomeres, chromosomes would fuse with each other. Telomere Shortening Telomeres shorten because of the two major factors:
 
  1. End replication problem in eukaryotes accounts for loss of 20 base pairs per cell division.
  2. Oxidative stress accounts for loss of 50-100 base pairs per cell division.
 
Figure 827.1
 
Oxidative stress in the body depends on lifestyle factors. Smoking, poor diet and stress can cause increase in oxidative stress. With each cell division telomeres shorten, so there are limited number of divisions that a cell can undergo, this limit is called Hayflick Limit. This is to prevent the loss of vital DNA information and to prevent production of abnormal cells. When a cell reaches this limit it undergoes apoptosis that is a programmed cell death. Telomere Lengthening to reverse telomere shortening, there is an enzyme named Telomerase that adds telomere sequence nucleotides and replenish the lost telomere nucleotides. Telomerase activity is not present in all cells. It is almost absent in somatic cells including; lung, liver, kidney cells, adult tissues, cardiac and skeletal muscles etc. In the presence of telomerase enzyme, a cell can divide to unlimited extent without ageing giving rise to tumors. That’s why it is found only in some cells in considerable concentration including germline cells and stem cells. These cells don’t show signs of ageing.
 
Figure 827.3
 
Relation between Telomere’s Shortening and Ageing
 
Figure 827.2It is still controversial that whether telomere shortening is a reason of ageing or is a sign of ageing just like grey hair. Whatever it is, the thing is, it determines your physiological age because ageing cells mean an ageing body. Telomere shortening is related with poor lifestyle. People who are active and have a healthy lifestyle have the same telomere length as someone 10 years younger than them has. Depression causes increase in oxidative stress in the body so the higher the stress, the shorter the telomere is Link between Telomeres and Cancer “Cancer in general is defined as an uncontrollable rapid growth of cells.”
 
What causes these cells to grow uncontrollably?
 
These cells have active telomerase enzyme, which doesn’t let the telomere to shorten, so no Hayflick limit reaches and cell continues to divide. This is the reason why telomerase is not used as an anti-ageing medicine because it has potential to turn normal body cells into cancerous cells. Without telomerase activity cancer cells activity would stop, which is an under research treatment for cancer. However, drugs inhibiting telomerase activity, can interfere with normal functioning of cells that require telomerase. In healthy female breast there is a portion of cells named, luminal progenitors, with critically short telomere length. In these cells telomerase becomes active causing these cells to turn into cancer cells on higher activity. To tackle breast cancer, use of telomerase inhibiting drugs should be practiced. Telomere biology is very important for understanding cancer biology and scientists are working hard on it.
 
 
Reviewed by Dr. Nida Hayat Khan
Editor @ BioScience.pk 
Fluorescence
 
A fluorochrome absorbs light energy and emits excess energy in the form of photon light (fluorescence). Fluorescence is the property of molecules to absorb light at one wavelength and emit light at a longer wavelength. The fluorescent dyes commonly used in flow cytometry are fluorescein isothiocyanate (FITC) and phycoerythrin (PE). The fluorochrome-labeled antibodies are used for detection of antigenic markers on the surface of cells. A particular cell type can be identified on the basis of the antigenic profile expressed. Multiple fluorochromes can be used to identify different cell types in a mixed population of cells.
 
Light Scatter
 
Light is scattered when the incident light is deflected by a particle traversing through a beam of light. This depends on the physical properties of the cell. Two forms of light scatter are used to identify different cell types: forward scatter and side scatter. Forward scatter (light scattered in the same direction as the laser beam) is related to cell size. Side scatter (light scattered at a 90° angle to the laser beam) is related to internal granularity of the cell. Main subpopulations of leukocytes are identified on the basis of correlated measurements of forward and side scatters. When a cell passes through laser beam, side scatter and fluorescent signals that are emitted by the cell are directed to photomultiplier tubes, while the forward scatter signals are directed to a photodiode. Photomultiplier tubes and photodiodes are called as detectors. Optical filters are placed before the detectors that allow only a narrow range of wavelengths to reach the detectors (see Figure 806.1).
 
Figure 806.1 Principle of working of a flow cytometer
Figure 806.1 Principle of working of a flow cytometer
 
Data Analysis
 
The data collected and stored in the computer can be displayed in various formats. A parameter means forward scatter, or side scatter, or emitted fluorescence from a particle as it passes through a laser beam. A histogram is a data plot of a single parameter, with the parameter’s signal value in channel numbers or relative fluorescence intensity on X-axis (horizontal axis) and number of events on the Y-axis. A dot plot is a two parameter data graph in which each dot represents one event that the flow cytometer analyzed; one parameter is displayed on the X-axis and the other on the Y-axis. A 3-D plot represents one parameter on X-axis, another parameter on Y-axis, and number of events per channel on Z-axis.
 
Gating
 
A gate is a boundary that can be set to restrict the analysis to a specific population within the sample. For example, a gate boundary can be drawn on a dot plot or histogram to restrict the analysis only to cells with the size of lymphocytes. Gates can be inclusive (selection of events that fall within the boundary) or exclusive (selection of events that fall outside the boundary). Data selected by the gate is then displayed in subsequent plots.
 
Sorting
 
Usually, when a cell passes through the laser beam, it is sent to waste. Sorting consists of collecting cells of interest (defined through criteria of size and fluorescence) for further analysis (such as microscopy or functional or chemical analysis). Sorting feature is available only in some flow cytometers.
The International Council for Standardization in Haematology (ICSH) was initiated as a standardization committee by the European Society of Haematology (ESH) in 1963 and officially constituted by the International Society of Hematology (ISH) and the ESH in Stockholm in 1964. The ICSH is recognised as a Non-Governmental Organisation with official relations to the World Health Organisation (WHO).
 
The ICSH is a not-for-profit organisation that aims to achieve reliable and reproducible results in laboratory analysis in the field of diagnostic haematology.
 
The ICSH coordinates Working Groups of experts to examine laboratory methods and instruments for haematological analyses, to deliberate on issues of standardization and to stimulate and coordinate scientific work as necessary towards the development of international standardization materials and guidelines.
Prickly heat usually clears up on its own within a few days. However, in serious cases heat rash can interfere with the body's heat-regulating mechanism and cause heat exhaustion.
 
Heatstroke is a more serious condition when the body can no longer cool itself. This is a medical emergency.
 
What causes prickly heat rash?
 
Heat rash begins with excessive perspiration, usually in a hot, humid environment. The perspiration makes it easier for dead skin cells and bacteria on the skin to block the sweat glands, forming a barrier and trapping sweat beneath the skin, where it builds up, causing the characteristic bumps. As the bumps burst and sweat is released, there may be a prickly, or stinging sensation that gives this condition its name.

What are the symptoms of heat rash?
 
Small, itchy red bumps on the skin are the symptoms of heat rash. The rash may feel prickly, stinging or burning.
 
Seek medical advice if:
 
  • Heat rash does not go away on its own within a few days.
  • You develop an infection in an area where you recently had heat rash.
 
What are the treatments for heat rash?
 
In most cases, heat rash will clear up on its own in a few days if the affected area is kept cool and dry. Avoid excessive heat and humidity and cool off with a fan, take a cool shower or bath and let your skin air dry, or if you have air-conditioning, use this to cool yourself. Once the skin is cool and dry again, don’t use any type of oil-based product, which might block your sweat glands. Calamine lotion and/or hydrocortisone cream can relieve itching and irritation.
 
If your prickly heat does not go away within a few days, or if you develop an infection where the bumps have burst, you may need medication, so seek medical advice.

How can I prevent heat rash?
 
To prevent heat rash, avoid situations that can lead to excessive sweating, such as hot, humid environments and strenuous physical activity. In hot weather, use fans and cool showers and baths to stay cool, or air conditioning if available; dry your skin thoroughly; and wear lightweight, loose-fitting clothes ideally made from cotton.
  • Allen’s LawAllen
  • Artificial ParthenogenesisLoeb
  • Axial Gradient theoryChild
  • Bergman’s RuleBergman
  • Biogenetic LawEarnst Haeckel (1868)
  • Biological Species ConceptEarnst Mayer
  • Biogenesis TheoryDeveloped by F. Redi
  • Chromosomal Theory of InheritanceSutton and Boveri
  • Theory of natural selectionCharles Darwin

Amino acid sequence of protein (insulin)
Sanger

Anaerobic release of energy
L-Pasteur (1878)

Bacteria
Leeuwenhoek

Pure culture of Bacteria
Lister J.

Bacteriophage
Towrt and De Herelle (1915)

Blood Capillaries
Marcello Malpighi

Blood Groups
Karl Landsteiner

Blood Circulation
William Harvey

Bioluminescence
E.R. Dubois

Biocatalysts
Buchner

Cyanophage
Saffermann and Morris

First description of cell (RBC)
Jan Swammerdam (1658)

Cell
Robert Hooke (1665)

Living cell
A.V. Leeuwenhoek

Cell Theory
Schleiden and Schwann

Centrosome
Van Benden

Centriole
Van Benden

Chromosomes
Hofmeister

Golgi bodies
Cammileo Golgi

Plastids
Haeckel (1866)

Chioroplast
Schimper

Mitochondria
Kolliker (1880)

Microtubules
Robertis and Francis

Microfilaments
Paleviz et. al (1975)

Nucleus
Robert Brown

Nucleolus
Fontana

Nucleoplasm
Strasburger

Ribosomes (Animal cell)
Palade

Sphaerosome
Pernes (1953)

Astral rays and spindle
Beevers

Endoplasmic reticulum
Porter

Central Dogma
F.H.C. Crick (1918)

Coenzyme A
C. Lipmann

Chlorophyll structure
Willstartter and Fisher

Cyclosis
Amid

Cytochrome
C.A. Macmunn (1886)

Citric Acid cycle
Hans A. Krebs

Double Helical Structure of DNA
Watson and Crick

Biological Synthesis of DNA with template
A. Kornberg.

biological synthesis of DNA without template
H.G. Khorona

Enzyme
Buchner

Embryo culture
Laiback

Extra embryonic membranes
Von Baer

Fertilization in plants
E. Strasburger

Double fertilization
Nawaschin

Go phase
Lajtha

Gaseous exchange in blood
Ludwig (1872)

Genetic defects in human
Sir Archibald Garrod

Giant Salivary gland chromosomes
Balbiani (1881)

Hormones
Beylis and Starling

Heterothallism
Blackslee

Interferon
Issacs and Linderman

Insulin use for treatment of diabetics
Banting

Mendelism
G. Mendel

Rediscoverer of Mendelism
Correns, Hugo de Vries and Tschmark

Microtome
W. His

Micro-organisms
Leeuwenhoek

Mitosis
W. Flemming

Meiosis
Farmer and Moore

Mutations
Hugo de Vries

Nucleic acid
Meishcher called it ‘Nuclein’

Ovum (Mammalian)
Karl E. Von Baer

Omnis cellula e cellula
R. Virchow

Pinocytosis
Edward and Lewis

Phagocytosis
Metchnikoff

Penicillin
Alexander Flemming

Plasmodesmata
Strasburger

Photorespiration
Garner and Allard

Quantosome
Park and Bigginis (1960)

Quiescent centre
Clowes

Protoplasm Physical basis of life
Huxley

Streptomycin
Salmon Waksman

Techniques Chromatograph
M. Tswett

Tissue culture
A. Carrel

Isotopic tracing
G. Havesy

Measuring gaseous exchange manometry
O. Warburg

Locating DNA in cell
A. Feulgen

Ultracentrifugation
T. Svedberg

Avena curvature test
Went

Teminism (Reverse Transcription)
Temin

Synthesis of urea
Wohler

Virus
D. Iwanovsky

Obtained crystals of virus
Stanley

Antileprosy day
30th Jan

International Women day
8th March

World Handicaps day
15th March

World Forest day
21st March

World Tuberculosis day
26th March

World Health day
7th April

World Earth day
22nd April

International Sun day (Non-conventional Energy sources day)
3rd May

World Red Cross day
8th May

World No Tobacco Day
31st May

World Environment day
5th June

World Population Day
11th July

Hiroshima and Nagasaki Day
6th Aug

Malaria day (mosquito day)
20th Aug

Blood Donation Day
1st Oct

World Animal Day
3rd Oct

World habitat Day
4th Oct

World Food Day
16th Oct

World Diabetes Day
14 Nov

World AIDS Day
1st Dec

National Pollution Prevention Day
2nd Dec

World conservation Day
3rd Dec

International Day for Biological Diversity
29th Dec

  • Abdul Qadir Khan Research Laboratories
  • Energy Conservation Cell (ENERCON), Islamabad
  • Drainage Research Institute of Pakistan (DRIP), Hyderabad
  • Forestry Institute, Peshawar
  • Ghulam Ishaq Khan Institute of Advanced Science and Technology, Tarbella
  • Geological Survey of Pakistan, Rawalpindi
  • Irrigation, Drainage, and Flood Control Research Council, Islamabad
  • National Center for Technology Transfer (NCTT), Islamabad
  • National Institute of Health (NIH), Islamabad
  • Nuclear Institute of Agricultural Biology (NIAB), Faisalabad
  • Pakistan Agricultural Research Council (PARC), Islamabad
  • Pakistan Arts Council
  • Pakistan Atomic Energy Commission (PAEC), Islamabad
  • Pakistan Council of Industrial and Scientific Research (PCSIR)
  • Pakistan Science Foundation (PSF), Islamabad
  • Pakistan Health Research Council (PHRC), Islamabad
  • Silicon Institute of Technology, Islamabad
  • Space and Upper Atmosphere Research Council (SUPPARCO), Karachi

Har Gobind Khorana was born of Hindu parents in Raipur, a little village in Punjab, which is now part of eastern Pakistan. The correct date of his birth is not known; that shown in documents is January 9th, 1922. He is the youngest of a family of one daughter and four sons. His father was a «patwari», a village agricultural taxation clerk in the British Indian system of government. Although poor, his father was dedicated to educating his children and they were practically the only literate family in the village inhabited by about 100 people.

Har Gobind Khorana attended D.A.V. High School in Multan (now West Punjab); Ratan Lal, one of his teachers, influenced him greatly during that period. Later, he studied at the Punjab University in Lahore where he obtained an M. Sc. degree. Mahan Singh, a great teacher and accurate experimentalist, was his supervisor.

Khorana lived in India until 1945, when the award of a Government of India Fellowship made it possible for him to go to England and he studied for a Ph. D. degree at the University of Liverpool. Roger J. S. Beer supervised his research, and, in addition, looked after him diligently. It was the introduction of Khorana to Western civilization and culture.

Khorana spent a postdoctoral year (1948-1949) at the Eidgenössische Technische Hochschule in Zurich with Professor Vladimir Prelog. The association with Professor Prelog molded immeasurably his thought and philosophy towards science, work, and effort.

After a brief period in India in the fall of 1949, Khorana returned to England where he obtained a fellowship to work with Dr. (now Professor) G. W. Kenner and Professor (now Lord) A. R. Todd. He stayed in Cambridge from 1950 till 1952. Again, this stay proved to be of decisive value to Khorana. Interest in both proteins and nucleic acids took root at that time.

A job offer in 1952 from Dr. Gordon M. Shrum of British Columbia (now Chancellor of Simon Fraser University, British Columbia) took him to Vancouver. The British Columbia Research Council offered at that time very little by way of facilities, but there was «all the freedom in the world», to use Dr. Shrum's words, to do what the researcher liked to do. During the following years, with Dr. Shrum's inspiration and encouragement and frequent help and scientific counsel from Dr. Jack Campbell (now Head of the Department of Microbiology at the University of British Columbia), a group began to work in the field of biologically interesting phosphate esters and nucleic acids. Among the many devoted and loyal colleagues of this period, there should, in particular, be mention of Dr. Gordon M. Tener (now a Professor in the Biochemistry Department of the University of British Columbia), who contributed much to the spiritual and intellectual well-being of the group.

In 1960 Khorana moved to the Institute for Enzyme Research at the University of Wisconsin. He became a naturalized citizen of the United States. As of the fall of 1970 Khorana has been Alfred P. Sloan Professor of Biology and Chemistry at the Massachusetts Institute of Technology.

Har Gobind Khorana was married in 1952 to Esther Elizabeth Sibler, who is of Swiss origin. Esther brought a consistent sense of purpose into his life at a time when, after six years' absence from the country of his birth, Khorana felt out of place everywhere and at home nowhere. They have three children: Julia Elizabeth (born May 4th, 1953), Emily Anne (born October 18th, 1954), and Dave Roy (born July 26th, 1958).

Most adults carry multiple herpesviruses. Following the initial acute infection, these viruses establish life-long infections in their hosts and cause cold sores, keratitis, genital herpes, shingles, infectious mononucleosis, and other diseases. Some herpesviruses can cause cancer in man. During the latent phase of infection, the viruses remain dormant for long periods of time, but retain the capacity to cause occasional reactivations, that may lead to disease. A study published on June 30th in PLOS Pathogens suggests that attacking herpesvirus DNA with CRISPR/Cas9 genome editing technology can suppress virus replication and, in some cases, lead to elimination of the virus.

The CRISPR/Cas9 system targets specific DNA sequences and induces clean cuts across both strands of the DNA. In mammalian cells, such cuts are flagged and quickly repaired by an emergency repair system called NHEJ (for non-homologous end-joining). NHEJ is efficient but not very accurate and often results in insertion or deletion of a few DNA bases at the repair site. Because DNA is read in codons of three bases at a time, such small changes in critical positions often destroy the function of the respective gene and its protein product.

Robert Jan Lebbink, from the University Medical Center in Utrecht, The Netherlands, and colleagues reasoned that CRISPR/Cas9 could target and mutate latent herpesvirus DNA in infected human cells and so potentially prevent herpesvirus-associated diseases. To test this, the researchers devised specific guide (g)RNAs—sequences that are complementary to vital parts of the viral genome and function as 'molecular addresses'. These gRNAs, combined with the 'molecular scissors' part of the CRISPR/Cas9 system, should induce specific cuts and subsequent mutations in the herpesvirus DNA, and so cripple the viruses.

In their systematic approach, the researchers looked at three different members of the herpesvirus group: herpes simplex virus type 1 (HSV-1) causing cold sores and herpes keratitis; human cytomegalovirus (HCMV), the most common viral cause of birth defects (when the virus is transmitted from mother to fetus); and Epstein-Barr virus (EBV) causing infectious mononucleosis and multiple types of cancer.

Working with lymphoma cells latently infected with EBV, the researchers showed that introduction of gRNAs that target specific EBV DNA sequences can introduce mutations at the targeted sites. Such mutations can eliminate essential functions of the virus as well as de-stabilize the viral DNA molecules. Consistent with this, the researchers report that by using two different gRNAs targeting an essential EBV gene, they can induce loss of over 95% of EBV genomes from the host cells.

During latent infection, HCMV genomes exist as circular DNA molecules in the nucleus of host cells. Upon virus reactivation, HCMV replication proceeds slowly. With appropriate gRNAs, the researchers found that CRISPR/Cas9 editing can efficiently impair HCMV replication. However, they also observed emergence of escape variants that bypass CRISPR/Cas9 editing, suggesting that simultaneous editing at multiple critical sites in the HCMV genome is necessary to avoid the development of resistant genomes.

Compared to HCMV, HSV-1 multiplies much faster. When the researchers tested various gRNAs targeting different essential HSV-1 genes in conjunction with CRISPR/Cas9, they found that many of them were able to reduce virus replication. When they combined two of those gRNAs, thereby simultaneously targeting two essential genes, they were able to completely suppress HSV-1 replication. On the other hand, they were unable to induce editing during the latent phase, i.e. when the viral DNA was not actively multiplying.

"We observed highly efficient and specific clearance of EBV from latently infected tumor cells and impairment of HSV-1 and HCMV replication in human cells", the researchers summarize. They go on to say, "although CRISPR/Cas9 was inefficient at directing genome engineering of quiescent HSV-1, virus replication upon reactivation of quiescent HSV-1 was efficiently abrogated using anti-HSV-1 gRNAs". Their results, they hope, "may allow the design of effective therapeutic strategies to target human herpesviruses during both latent and productive infections."

Deadly Diseases

Humans have been battling viruses since before our species had even evolved into its modern form. For some viral diseases, vaccines and antiviral drugs have allowed us to keep infections from spreading widely, and have helped sick people recover. For one disease — smallpox — we've been able to eradicate it, ridding the world of new cases.
 
But as the Ebola outbreak now devastating West Africa demonstrates, we're a long way from winning the fight against viruses.
 
The strain that is driving the current epidemic, Ebola Zaire, kills up to 90 percent of the people it infects, making it the most lethal member of the Ebola family. "It couldn't be worse," said Elke Muhlberger, an Ebola virus expert and associate professor of microbiology at Boston University.
 
But there are other viruses out there that are equally deadly, and some that are even deadlier. Here are the nine worst killers, based on the likelihood that a person will die if they are infected with one of them, the sheer numbers of people they have killed, and whether they represent a growing threat.
 

1. Marburg virus

Scientists identified Marburg virus in 1967, when small outbreaks occurred among lab workers in Germany who were exposed to infected monkeys imported from Uganda. Marburg virus is similar to Ebola in that both can cause hemorrhagic fever, meaning that infected people develop high fevers and bleeding throughout the body that can lead to shock, organ failure and death.
 
The mortality rate in the first outbreak was 25 percent, but it was more than 80 percent in the 1998-2000 outbreak in the Democratic Republic of Congo, as well as in the 2005 outbreak in Angola, according to the World Health Organization (WHO).
 

2. Ebola virus

The first known Ebola outbreaks in humans struck simultaneously in the Sudan and the Democratic Republic of Congo in 1976. Ebola is spread through contact with blood or other body fluids, or tissue from infected people or animals. The known strains vary dramatically in their deadliness, Muhlberger said.
 
One strain, Ebola Reston, doesn't even make people sick. But for the Bundibugyo strain, the fatality rate is up to 50 percent, and it is up to 71 percent percent for the Sudan strain, according to WHO.
 
The outbreak underway in West Africa began in early 2014, and is the largest and most complex outbreak of the disease to date, according to WHO.
 

3. Rabies

Although rabies vaccines for pets, which were introduced in the 1920s, have helped make the disease exceedingly rare in the developed world, this condition remains a serious problem in India and parts of Africa.
 
"It destroys the brain, it's a really, really bad disease," Muhlberger said. "We have a vaccine against rabies, and we have antibodies that work against rabies, so if someone gets bitten by a rabid animal we can treat this person," she said.
 
However, she said, "if you don't get treatment, there's a 100 percent possibility you will die."
 

4. HIV

In the modern world, the deadliest virus of all may be HIV. "It is still the one that is the biggest killer," said Dr. Amesh Adalja, an infectious disease physician and spokesman for the Infectious Disease Society of America.
 
An estimated 36 million people have died from HIV since the disease was first recognized in the early 1980s. "The infectious disease that takes the biggest toll on mankind right now is HIV," Adalja said.
 
Powerful antiviral drugs have made it possible for people to live for years with HIV. But the disease continues to devastate many low- and middle-income countries, where 95 percent of new HIV infections occur. Nearly 1 in every 20 adults in Sub-Saharan Africa is HIV-positive, according to WHO.
 

5. Smallpox

In 1980, the World Health Assembly declared the world free of smallpox. But before that, humans battled smallpox for thousands of years, and the disease killed about 1 in 3 of those it infected. It left survivors with deep, permanent scars and, often, blindness.
 
Mortality rates were far higher in populations outside of Europe, where people had little contact with the virus before visitors brought it to their regions.  For example, historians estimate 90 percent of the native population of the Americas died from smallpox introduced by European explorers. In the 20th century alone, smallpox killed 300 million people.
 
"It was something that had a huge burden on the planet, not just death but also blindness, and that's what spurred the campaign to eradicate from the Earth," Adalja said.
 

6. Hantavirus

Hantavirus pulmonary syndrome (HPS) first gained wide attention in the U.S. in 1993, when a healthy, young Navajo man and his fiancée living in the Four Corners area of the United States died within days of developing shortness of breath. A few months later, health authorities isolated hantavirus from a deer mouse living in the home of one of the infected people. More than 600 people in the U.S. have now contracted HPS, and 36 percent have died from the disease, according to the Centers for Disease Control and Prevention.
 
The virus is not transmitted from one person to another, rather, people contract the disease from exposure to the droppings of infected mice.
 
Previously, a different hantavirus caused an outbreak in the early 1950s, during the Korean War, according to a 2010 paper in the journal Clinical Microbiology Reviews. More than 3,000 troops became infected, and about 12 percent of them died.
 
While the virus was new to Western medicine when it was discovered in the U.S., researchers realized later that Navajo medical traditions describe a similar illness, and linked the disease to mice.
 

7. Influenza

During a typical flu season, up to 500,000 people worldwide will die from the illness, according to WHO. But occasionally, when a new flu strain emerges, a pandemic results with a faster spread of disease and, often, higher mortality rates.
 
The most deadly flu pandemic, sometimes called the Spanish flu, began in 1918 and sickened up to 40 percent of the world's population, killing an estimated 50 million people.
 
"I think that it is possible that something like the 1918 flu outbreak could occur again," Muhlberger said. "If a new influenza strain found its way in the human population,and could be transmitted easily between humans, and caused severe illness, we would have a big problem."
 

8. Dengue

Dengue virus first appeared in the 1950s in the Philippines and Thailand, and has since spread throughout the tropical and subtropical regions of the globe. Up to 40 percent of the world's population now lives in areas where dengue is endemic, and the disease — with the mosquitoes that carry it — is likely to spread farther as the world warms.
 
Dengue sickens 50 to 100 million people a year, according to WHO. Although the mortality rate for dengue fever is lower than some other viruses, at 2.5 percent, the virus can cause an Ebola-like disease called dengue hemorrhagic fever, and that condition has a mortality rate of 20 percent if left untreated.
 
"We really need to think more about dengue virus because it is a real threat to us," Muhlberger said. There is no current vaccine against dengue, but large clinical trials of an experimental vaccine developed by French drug maker Sanofi have had promising results.
 

9. Rotavirus

Two vaccines are now available to protect children from rotavirus, the leading cause of severe diarrheal illness among babies and young children. The virus can spread rapidly, through what researchers call the fecal-oral route (meaning that small particles of feces end up being consumed).
 
Although children in the developed world rarely die from rotavirus infection, the disease is a killer in the developing world, where rehydration treatments are not widely available.
 
The WHO estimates that worldwide, 453,000 children younger than age 5 died from rotavirus infection in 2008. But countries that have introduced the vaccine have reported sharp declines in rotavirus hospitalizations and deaths.
Author: Anne Harding, Contributing Writer
Source: Live Science
Abstract: There are many factors that contribute to accurate test results in the chemistry laboratory. These factors can be broken down into three areas: preanalytical, analytical and post analytical. Preanalytical variables account for 32-75% of laboratory errors, and encompass the time from when the test is ordered by the physician until the sample is ready for analysis.1 The focus of this article will be preanalytical variables that can occur during a venipuncture and specimen processing and how they relate to testing in the clinical chemistry laboratory.
 
Scenario: A patient has been in the cardiac intensive care unit for 3 days. For the past 2 mornings, he has had his cardiac enzymes drawn into a BD SSTT tube to monitor his condition since his heart attack. On this particular morning, his tube of blood is drawn and sent to the clinical chemistry lab for analysis. However, when the tube is processed and ready for analysis, the technologist running the chemistry analyzer notices that the specimen is very gelatinous and will need to be re-processed before the sample can be run on the analyzer. What could have happened to the quality of this specimen?
There are many variables that can contribute to the quality of a chemistry specimen. This article will investigate the variables that may have contributed to the gelatinous specimen in the case of the cardiac patient, as well as the other variables that are important to specimen quality. The focus will be on the preanalytical phase of the blood collection and sample handling, up until the time that the sample is to be run on the chemistry instrument.
Following the above BD SST™ tube from time of collection until it is ready for analysis, the preanalytical variables that can contribute to the quality of the sample are as follows:
 
Patient Identification: It is important to identify a patient properly so that blood is being collected from the correct person. Drawing blood from the wrong person, or labeling the correct patient’s sample with a different patient’s label can certainly contribute to laboratory error. Perhaps in the opening scenario, the patient in the next bed, with an extremely prolonged clotting time, was drawn and labeled as the cardiac patient.
When identifying the patient, have them provide their full name, address, identification number and/or date of birth.2 Hospital inpatients should be wearing an identification band with the above information, which the phlebotomist should confirm before the venipuncture. Blood should not be drawn from a patient without a band. A nurse, physician, relative or guardian should identify patients that are unable to speak or identify themselves.
 
Patient Preparation: Prior to collecting specimens for chemistry, certain patient variables need to be considered. For certain chemistry analytes, such as glucose and cholesterol, patients need to be fasting (absence of food and liquids) for at least 12 hours prior to venipuncture. Other analytes, such as cortisol and adrenocorticotropin, have diurnal variations, where the analyte is at its highest level in the morning, and the levels gradually decrease during the course of the day.
 
Selecting the Site: Selecting the appropriate site for venipuncture can contribute to a better quality sample. The preferred site is the median cubital vein. This vein is usually the easiest to access. Generally, there is less need to probe to find the vein, which in turn should cause less trauma during the venipuncture. This will usually be the most comfortable for the patient. If the median cubital vein cannot be used, the next choice would be the cephalic vein. The last vein to consider for venipuncture is the basilic vein. This vein is in close proximity to the median nerve and brachial artery, and extreme caution must be used so that only the basilic vein is being punctured.
 
Site Preparation: Prior to venipuncture, the site should be cleansed with alcohol. Cleansing starts at the center of the vein, and should continue outward in concentric circles. Before performing the venipuncture, the alcohol should be allowed to air dry. This will help to ensure that the specimen is not contaminated with alcohol, as this can lead to hemolysis. Hemolysis can result in the spurious elevation of such analytes as potassium, lactate dehydrogenase (LD), iron and magnesium in the chemistry lab. Allowing the alcohol to dry completely will also cause less burning and pain to the patient.
 
Tourniquet Application and Time: The tourniquet should be applied approximately three to four inches above the venipuncture site. The tourniquet should be on the arm no longer than one minute. 2 A good rule of thumb to determine the one-minute tourniquet time is to remove the tourniquet when blood starts to flow into the first tube of blood being drawn. Prolonged tourniquet time can lead to an increase in various chemistry analytes, including serum protein, potassium and lactic acid due to hemoconcentration of blood at the puncture site.
 
Proper Venipuncture Technique: During phlebotomy, avoid probing to find the vein and achieve blood flow. Excessive probing and/or “fishing” to find a vein can result in a poor quality sample, including hemolysis. As mentioned previously, hemolysis can affect several chemistry analaytes.
 
Order of Draw: Following the correct order of draw during venipuncture will help to ensure accurate test results. The BD and CLSI (Clinical and Laboratory Standards Institute, formerly NCCLS) recommended order of draw for evacuated blood collection tubes is as follows (PDF).2
An example of improper order of draw that can lead to an incorrect chemistry result is drawing an EDTA tube prior to an BD SST ™ or heparin tube for chemistry testing. The potential cross contamination of K2 or K3EDTA on the needle from the lavender top tube to the chemistry tube can lead to an elevated potassium result. This in turn can require a recollection of the sample, or possible misdiagnosis or treatment of the patient.
 
Proper Tube Mixing: All tubes with additives need to be inverted to mix the additive evenly with the blood. Plastic serum tubes and BD SST™ tubes contain clot activator and should be inverted 5 times to mix the activator with the blood and help the specimen clot completely. In the opening case study, improper mixing of the tube after venipuncture could have contributed to the gelatinous serum sample that was seen in the laboratory. Other additive tubes, such as heparin, need to be inverted 8-10 times to mix the anticoagulant with the blood and prevent clotting. Be sure that tubes are not being shaken vigorously, as this can lead to a hemolyzed sample.
 
Correct Specimen Volume: All blood collection tubes need to be filled to the correct volume.3 This will ensure the proper amount of blood for the amount of additive in the tube (blood to additive ratio). For example, if a 5 mL draw heparin tube is only filled with 3 mL of blood, the heparin concentration is erroneously high and may potentially interfere with some chemistry analytes. Expiration dates should also be checked on the evacuated tubes.4 Expired tubes should not be used, as they may have a decreased vacuum, as well as potential changes in any additives in the tubes.
 
Proper Tube Handling and Specimen Processing: Once the blood collection tubes have been drawn in the correct order, to the proper fill volume and mixed thoroughly, the next step toward accurate test results is processing the tubes properly. This section will look at serum and plasma tubes separately, as both specimen types have their own special handling requirements.
 
Serum Samples
Serum specimens, namely red top tubes and BD SST™ gel tubes, need to clot completely prior to centrifugation and processing. Blood specimens in red top tubes should clot for 45 to 60 minutes, and those in BD SST ™ tubes should be allowed to clot for 30 minutes to ensure complete clot formation.4 Blood from patients who are receiving anticoagulant therapy, such as heparin or coumadin, may take longer to clot. Tubes should be allowed to clot at room temperature, upright in a test tube rack, with the closures on the tubes. In the gelatinous sample that was presented at the beginning of this article, perhaps the blood was not clotted completely prior to centrifugation because a cardiac patient is often heparanized. Spinning the tube too soon may result in a gelatinous and/or fibrinous serum sample that will require respinning.
 
Plasma Samples
Blood specimens collected in plasma tubes, such as the plain heparinized green top tubes and the BD PST™ tubes with heparin and gel do not require clotting prior to centrifugation. This allows the tube of blood to be drawn, mixed and centrifuged immediately, resulting in a quicker turn-around-time for test results.
 
Centrifugation: The next step in sample processing is the centrifugation of the blood collection tubes. Both BD SST™ and BD PST™ tubes are centrifuged at the same speed and for the same amount of time. In a swinging bucket centrifuge (preferred type of spin for gel separation tubes), the tubes should be spun for ten minutes at a speed of 1100 to 1300 relative centrifugal force (RCF). A fifteen-minute spin at the same speed is required for spinning tubes in a fixed- angle centrifuge. Serum and plasma tubes without gel can be spun at a speed of 1000 RCF for ten minutes.4
It is important to spin gel tubes for the recommended time. The gel barrier in the tubes needs time to move and form a solid barrier between the red cells and the serum or plasma. Also, in BD PST™ tubes, the white blood cells and platelets that remain in the plasma need adequate time to spin out of the plasma. If the BD PST™ tubes are spun for less than the recommended 10 minutes, these cells and platelets may remain in the plasma and could cause interference with some chemistry analytes. It is recommended that BD SST™ tubes should not be re-centrifuged after their initial centrifugation. Re-spinning the tubes can result in elevated potassium values, as excess serum that has been in contact with the red cells will be expressed from underneath the gel barrier.
 
Special Handling of Blood Specimens: Certain chemistry analytes will require the tube of blood to be chilled after collection in order to maintain the stability of the analyte. A slurry of ice and water is recommended for chilling the tubes of blood. Examples of specimens that need to be chilled or transported on ice include adrenocorticotropic hormone (ACTH), angiotensin converting enzyme (ACE), acetone, ammonia, catecholamines, free fatty acids, lactic acid, pyruvate and renin.
Other anayltes are photo-sensitive, and need to be protected from light in order to remain stable and to ensure that the laboratory reports an accurate result. This can be done by wrapping the tube of blood in aluminum foil. The most common example of a light-sensitive analyte is bilirubin. Other chemistry analytes that need to be light-protected include beta-carotene and erythrocyte protoporphyrin.
 
Stability for Whole Blood, Serum and Plasma: A whole blood specimen that is going to be spun down should be centrifuged and the serum or plasma removed from the red blood cells within two hours after the venipuncture.5 Once the serum has been removed or separated from the red blood cells (in the case of a gel barrier tube), the sample will be stable at room temperature for eight hours, and up to 48 hours at 2-4 degrees C.5 After 48 hours, the serum specimen should be frozen at –20 degrees C in an aliquot tube.5
Paying close attention to the preanalytical variables associated with blood collection will help to ensure accurate test results in the chemistry department, as well as all areas of the clinical laboratory. As was evident from the opening case study, there are often several variables that can potentially contribute to erroneous test results. Our cardiac patient’s blood could have been drawn from the wrong patient, had improper tube handling or his blood may have not clotted long enough. Therefore, it is important to remember that a better quality sample during the preanalytical phase of blood collection will yield a better test result.
 
References
1. Bonini P, PlebaniM, Ceriotti F, et al. Errors in laboratory medicine. Clin Chem. 2002;48:691-698.
2. NCCLS – Procedures for the Collection of Diagnostic Blood Specimens by Venipuncture; Approved Standard, Fifth Edition, H3-A5 Vol. 23 No. 32, December 2003.
3. NCCLS – Tubes and Additives for Blood Specimen Collection; Approved Standard-Fifth Edition, H1- A5 Vol. 23 No. 33, December 2003.
4. BD Evacuated Blood Collection System Package Insert 6/2004
5. NCCLS – Procedures for the Handling and Processing of Blood Specimens; Approved Standard-Third Edition, H18-A3 Vol. 24 No. 38, November 2004.
An affordable, widely available test can impact today`s biggest healthcare challenge.
 
Sepsis, the inflammatory response to infection, is quickly becoming one of the biggest healthcare problems worldwide. No matter the perspective one takes, the numbers are staggering. Currently the number of diagnosed cases per year in the United States is at least 750,000; some estimates surpass one million. Worldwide mortality estimates are as high as 20 percent, and thus we are dealing with one of the biggest drivers of mortality in modern medicine. Sepsis kills nearly as many people as heart attack, HIV, and breast cancer combined.
 
Viewed from the perspective of health economics, the average in-hospital cost per case is approximately $20,000 dollars, and yearly estimates of sepsis-related expenses in the U.S. alone exceed $20 billion.
 
To compound an already dire situation, all predictive models indicate steady increases in sepsis prevalence over the next years and decades, as the risk factors typically linked to sepsis become ever more prevalent: The proportion of elderly patients in the general population is increasing; the number of patients living with chronic health problems such as diabetes, cancer, and chronic renal failure, among others, is increasing; and the number of patients taking immunosuppressant therapies for a variety of reasons is also on the rise. Put these together and there is a perfect storm brewing, and healthcare systems and providers, among them pathologists and laboratories, must be ready to respond.
In order to prepare, it is critical to understand how sepsis patients enter healthcare pathways, and where key opportunities to improve outcomes lie. Literature on this topic yield some key findings which can guide healthcare institutions and providers in designing optimal strategies to deliver fast and effective care to their sepsis patients:
  • Sepsis patients typically enter healthcare pathways via the emergency department (ED) (approximately 70 percent of cases), or become septic during an intensive care unit (ICU) admission (approximately 25 percent). These two locations are critical target areas for optimizing early sepsis detection protocols.
  • The majority of patients who ultimately die of sepsis already are septic upon presentation at the ED.
  • The majority of patients who die of sepsis do not have more severe forms of sepsis (with documentation of end-organ failure) at presentation.
Taken together, these findings highlight the need for well-established early warning mechanisms to raise the suspicion of sepsis even in the earliest stages of the disease. The ideal location for the deployment of such mechanisms is the ED (including the laboratory services that target this patient population).
 
Improvements in sepsis outcomes
 
In the last decade, while sepsis incidences were sharply increasing, the good news was that patient outcomes were actually improving. Some studies demonstrated decreases from 18 percent to 12 percent in sepsis-associated hospital mortalities between 2004 and 2013. This success was due in great part to efforts such as those of the Surviving Sepsis Campaign, which raised awareness among treating physicians of the importance of having a high index of suspicion for the disease. In this effort, researchers documented that the most critical factor leading to improved outcomes in sepsis was the time to start effective antibiotics. One study showed that each hour of delay was associated with a 7.6 percent increase in mortality. With this data in mind, many institutions now have early sepsis detection protocols to ensure that these patients are recognized and treated quickly, and such protocols and increased awareness have been credited with bringing about the significant improvements in sepsis mortality.
 
However, now that sepsis is already being treated quickly and effectively once clinical suspicion arises, the challenge has moved elsewhere; in order to further improve outcomes, the goal now is to assist clinicians in suspecting sepsis sooner, ideally before the more obvious clinical signs and symptoms are present. And the hematology laboratory may play a critical role in addressing this new challenge in the sepsis arena.
 
How hematology can help
 
Today the laboratory plays only a limited role in the early detection of sepsis and the improvement of patient outcomes, for several reasons:
  • Lab tests for sepsis tend to have low specificity, as most current laboratory biomarkers of sepsis are also elevated in other inflammatory conditions, for example, systemic inflammatory response syndrome (SIRS).
  • The majority of recently proposed tests for sepsis (procalcitonin, lactate) are performed only when the clinician is already suspecting it (and thus is ordering the test). At this point, the sepsis protocol, including broad spectrum antibiotics, will be implemented anyway, and thus further improvements in patient outcomes are unlikely.
  • Cost constraints prevent the widespread utilization of these recently proposed biomarkers in the broad ED population, thus making them inadequately suited as early markers of sepsis (prior to clinical suspicion).
Sepsis researchers have recognized that any new biomarkers they propose will likely face similar constraints, especially if they are additional tests not routinely performed during the ED visit or ICU admission. Therefore, a new focus has emerged in studies trying to identify mechanisms for earlier suspicion of sepsis using data that is already available. In particular, laboratory data such as CBC-diff results, analyzed in new multi-parametric algorithms or using novel data not previously available for clinical use, are especially valuable, because they are readily available at a very low cost for the majority of patients visiting the ED or admitted at the ICU. Thus these “upgraded” CBC-diff results can be used as early warning biomarkers even before clinical suspicion would justify the ordering of more costly tests such as procalcitonin.
 
For these reasons, researchers have recently published numerous studies on new strategies to leverage already available CBC-diff data for early detection of sepsis. These strategies fall in two broad categories: multi-parametric algorithms, and utilization of cellular morphologic data.
 
Multi-parametric algorithms
 
Multi-parametric algorithms are logistic regression models which identify various parameters differing in two groups (in this case, sepsis versus non-sepsis), giving weight to each individual parameter based on the magnitude of the difference seen for that parameter, and using a mathematical formula including those weights to identify a final “factor” –an index result which predicts the likelihood of sepsis. The key challenge with this approach is reproducibility across patient populations; the more parameters one includes in the model, the less likely it is that results will be replicated at a different institution.
 
Another common mistake seen in this line of research has been the inclusion of non-hematological data in the models to increase the discriminating power (for example, other biomarkers such as procalcitonin, CRP, interleukins, and sometimes even patient clinical and demographic data). This is a mistake because these are not tests that are routinely available to most patients at the same time the CBC-diff is being performed, so an algorithm using them will have the same problem of multiple recently proposed biomarkers for sepsis which have not been widely adopted by clinicians; if you need to suspect sepsis first to order the test, the window of opportunity to further improve sepsis outcomes has already passed.
 
Cellular morphologic data
 
The utilization of cellular morphologic data is based on the recognition that leucocytes, when primed to fight infection, undergo key changes in various morphologic features such as their shape, size, cytoplasmic granularity, and even their pliability. In fact, these features have already been used for decades by pathologists and technologists while reviewing cells under the microscope, and findings such as toxic granulation, Dohle bodies, and cytoplasmic vacuolization are currently used to raise the suspicion that a patient is undergoing an infectious process regardless of the total and differential leucocyte counts. The key challenge in this approach is that only a small proportion of CBC-diff test orders ever lead to a microscopic review, and given current staff limitations, cost containment efforts, and increasing pressure for a very fast turnaround time of results, it is not feasible for laboratories to manually review all CBC-diff tests coming from ED patients in order to search for these morphologic features, no matter how diagnostically relevant they may be.
 
A key solution currently under investigation is the utilization of hematological analyzers which automatically quantify these morphologic features, so that they can be reported to clinicians as numerical parameters included in the routine CBC-diff results. This approach is already widely accepted in the red blood cell arena, where the mean cell volume (MCV) and the red blood cell distribution width (RDW) are part of the traditional CBC-diff results. It can offer clinicians critical insight into morphological features of red cells, so that they can further guide their diagnostic work-up, especially in anemic patients.
 
In summary, the hematology laboratory is perfectly positioned in the sepsis diagnostic pathway to become a key solution to further improve clinical outcomes in this disease. This is true because the CBC-diff is a test routinely ordered at very low cost for the majority of patients entering the ED or admitted at the ICU, the two main locations where early sepsis detection is critical. In order for this use of the CBC-diff to be realized, however, it is critical that researchers find better ways to use hematological data, because the traditional parameters reported today as part of the CBC-diff do not have the level of sensitivity and specificity needed to properly distinguish sepsis from the myriad of mimicking conditions that clinicians must include in their differential diagnoses.
 
The impact of new diagnostic criteria
 
A word of caution is needed, however, as the official criteria for sepsis diagnosis have recently changed. A task force of 19 leaders in the field of sepsis was convened by the Society for Critical Care Medicine and the European Society of Intensive Care Medicine to put forth new guidelines for sepsis diagnosis. While a full description of these changes is beyond the scope of this article, it is important to highlight how they impact the role of the laboratory in sepsis diagnosis.
 
In previous guidelines, sepsis was diagnosed when patients had clinical evidence of systemic inflammatory response, and a documented or suspected infection. “Severe sepsis” was diagnosed when end organ failure was also documented based on a set of clinical and laboratory tests for organ function (i.e., creatinine, bilirubin, platelet counts, among others).
 
In the new guidelines, the category “severe sepsis” was removed, and the diagnosis of sepsis itself now requires the recognition of a life-threatening organ dysfunction due to a disregulated host response to infection. This organ dysfunction is based on the “sequential organ failure score” (SOFA), which uses several laboratory parameters.
 
The key challenge to the hematology laboratory is that its greatest potential value is in the identification of early sepsis patients; those who don’t yet have end organ failure and thus could benefit most from early antibiotic therapy. Under the new guidelines, these patients will no longer be formally diagnosed as “septic.” Having said that, it is well recognized in the literature that these patients do have higher mortality rates compared with patients with simple infections not associated with a disregulated inflammatory response, and thus early identification of these patients remains critical to improve outcomes, regardless of the formal diagnosis they ultimately receive.
 
It is critical that laboratory medicine researchers and practicing pathologists consider the differences between the old and new sepsis guidelines in their decisions, and in particular that future studies continue to distinguish patient populations with simple infections from those who have associated disregulated inflammation, because prompt identification of the latter population is needed for early initiation of antibiotic therapy and overall improvements in sepsis-related outcomes.
 
References
  1. Liu V, Escobar GJ, Greene JD, et al. Hospital deaths in patients with sepsis from 2 independent cohorts. JAMA. 2014 Jul 2;312(1):90-92.
  2. Rhodes A, Phillips G, Beale Ret al.. The Surviving Sepsis Campaign bundles and outcome: results from the International Multicentre Prevalence Study on Sepsis (the IMPreSS study). Intensive Care Med. 2015;41(9):1620-1628.
  3. Levy MM, Dellinger RP, Townsend SR et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Intensive Care Med. 2010;36(2):222-2231.
  4. Lagu T, Rothberg MB, Shieh MS, Pekow PS, Steingrub JS, Lindenauer PK. Hospitalizations, costs, and outcomes of severe sepsis in the United States 2003 to 2007. Crit Care Med. 2012;40(3):754-761.
  5. Rivers E, Nguyen B, Havstad S, et al. Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM. 2001 Nov 8;345(19):1368-1377.
  6. Jones AE, Shapiro NI, Roshon M. Implementing early goal-directed therapy in the emergency setting: the challenges and experiences of translating research innovations into clinical reality in academic and community settings. Acad Emerg Med 2007;14:1072-1078.
  7. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 200634(6):1589-1596.
  8. ProCESS Investigators, Yealy DM, Kellum JA, Huang DT, et al. A randomized trial of protocol-based care for early septic shock. NEJM. 2014 May 1;370(18):1683-1693.
  9. Tang BM, Eslick GD, Craig JC, McLean AS. Accuracy of procalcitonin for sepsis diagnosis in critically ill patients: systematic review and meta-analysis. Lancet Infect Dis. 2007;7(3):210-217.
  10. Pierrakos C, Vincent JL. Sepsis biomarkers: a review. Crit Care. 2010;14(1):R15.
  11. Nierhaus A, Linssen J, Wichmann D, Braune S, Kluge S. Use of a weighted, automated analysis of the differential blood count to differentiate sepsis from non-infectious systemic inflammation: the intensive care infection score (ICIS). Inflamm Allergy Drug Targets. 2012;11(2):109-1015.
  12. Crouser ED, Parrillo J, Angus D, et al. A feasibility trial to detect sepsis in the ED based upon blood monocyte volume variability. Society of Critical Care Medicine’s (SCCM) 45th Critical Care Congress: Abstract 58. Presented February 21, 2016. http://www.medscape.com/viewarticle/859717.
  13. Singer M, Deutschman CS; Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315 (8):801-810.

Fernando Chaves, MD, serves as Director, Global Scientific Affairs, Beckman Coulter Diagnostics. | Source: MLO

From Wikipedia, the free encyclopedia

Bioscience, Biotechnology, and Biochemistry is a monthly, peer-reviewedscientific journal published by the Japan Society for Bioscience, Biotechnology and Agrochemistry, of which it is the official journal. It was established in 1924 as Bulletin of the Agricultural Chemical Society of Japan, which was renamed to Agriculture and Biological Chemistry in 1961. The journal took its current name in 1991.

Scope

The focus of Bioscience, Biotechnology, and Biochemistry is previously unpublished original research results on all topics and fields concerning bioscience, biotechnology, and biochemistry. In addition, articles cover basic and applied sciences regarding microorganisms, including systems supporting their production, and structure. Broad topical coverage includes organic chemistry, bioorganic chemistry, physical chemistry, analytical chemistry, enzymology, biopolymer science, microbiology (including virology), animal science, plant science, food science, and environmental science.

Research applications are directed toward human welfare in general. Hence applications are transferred to industries of fermentation, chemistry and biochemistry, medicines and pharmaceuticals, foods and feeds, and agriculture.

Abstracting and indexing

Bioscience, Biotechnology, and Biochemistry is indexed in the following databases.

According to the Journal Citation Reports, it has an impact factor of 1.063 for 2014.

References

  1. "Agricultural and Biological Chemistry". Literature / Source Database. European Virtual Institute for Speciation Analysis. Retrieved 2010-08-19.
  2. "Agricultural and Biological Chemistry". Library of Congress Online Catalog. Library of Congress. Retrieved 2010-08-19.
  3. "Bioscience, Biotechnology, and Biochemistry".Literature/Source database. European Virtual Institute for Speciation Analysis. Retrieved 2010-08-19.
  4. "An Introduction to the Japan Society for Bioscience, Biotechnology and Agrochemistry". Academy of Science, Fields of Research, Contributions. JSBBA. August 2010. Retrieved 2010-08-19.

Navigation menu

A simple explanation to the question "If humans evolved from monkeys, then why are there still monkeys?" (Infographic courtesy of user "slipperyfish" from reddit.com.)
 
ubZNn
 
Claim- Drinking a cold glass of water after a meal can harm you. The cold water will solidify the oily stuff that you have just consumed, which will line the intestines and lead to cancer.
 
5joav
Is that Bovine Waste Matter I smell?
 
Verdict- False. Even if you accepted these claims as truth, a statement such as "A cardiologist says if you forward this to 10 people..." should have set off any properly working bullshit meter with a host of bells and flashing red lights. When you drink cold water, it is entering a system that self regulates to keep its core temperature within about half a degree, or around 37 c (98.6 f). ( For those that are wondering, typical oral temperature readings should be slightly cooler at 36.8c (96.2f)). From the time the water first comes into contact with your body, the heat transfer will begin to warm it up, and it will equalize within a few minutes. As an added bonus, drinking a half liter of ice cold water will actually make your body burn around 17 Calories in order to keep its temperature constant. The meal that you just consumed will not be affected in any way, as it will still end up at around the same temperature right up until you... uh "drop it off at the pool", regardless if you decided to wash it down with coffee or ice water afterwards.
 
Ipivu
Evil Ambitions?
 
Clogged large intestines do not cause cancer, they are a sign of cancer. Cancer is an uncontrolled division of abnormal cells in a part of the body. One way to think of it is when your cells replicate, a small error suddenly occurs in the copy process. That error gets passed down to the next copy and the next copy and the next. Before you know it, that one erroneous cell is now 2, then 4, then 16, then 256... eventually replacing all the good cells with cheap knock offs, and before long you're shopping for replacement parts because the original one(s) can no longer function the way it was meant to. (Sorry for the bad analogy. I think I have been working on cars too much lately.) Don't worry too much if you're feeling a little clogged up though because there are many other reasons for blockage, and most can be solved with a little bit of fiber in your diet.
 
0T7sA
A Donor Heart Waiting For The Doctor To Get Back From The Golf Course.
 
The heart attack information is reasonably accurate but a little incoherent. Jaw pain may be a symptom of a heart attack, but typically accompanying other symptoms. The American Heart Association's warning signs your ticker may be faulty include;
  • Uncomfortable Pressure, a squeezing or pain in the middle of your chest lasting for more than a few minutes
  • Mild to intense pain spreading to the shoulders, arms, or neck, or jaw.
  • Chest discomfort, feeling light headed, fainting, sweating, nausea, shortness of breath. Anxiety, nervousness, cold or sweaty skin, irregular heart rate,
Not all of these signs will necessarily occur. If you have one or more of these signs it is recommended you seek medical attention immediately, or you're going to end up having a really bad time.
 

Resources:
  1. Snopes Cold Water Myth * http://www.snopes.com/medical/myths/coldwater.asp
  2. Human Body Temperature * http://en.wikipedia.org/wiki/Human_body_temperature
  3. Heart Attack Symptoms And Signs * http://www.healthcentral.com/heart-disease/patient-guide-44510-6.html
  4. Bowel Obstruction Symptoms And Causes * http://www.webmd.com/digestive-disorders/tc/bowel-obstruction-topic-overview

Dictionary:

Our Sponsors