prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What molecule was the focus of the study?

Read the following text and answer briefly.

Context 1: \section{Introduction}

Spectral line surveys have revealed that high-mass star-forming
regions are rich reservoirs of molecules from simple diatomic species
to complex and larger molecules (e g ,
\citealt{schilke1997b,hatchell1998b,comito2005,bisschop2007}) 
However, there have been rarely studies undertaken to investigate the
chemical evolution during massive star formation from the earliest
evolutionary stages, i e , from High-Mass Starless Cores (HMSCs) and
High-Mass Cores with embedded low- to intermediate-mass protostars
destined to become massive stars, via High-Mass Protostellar Objects
(HMPOs) to the final stars that are able to produce Ultracompact H{\sc
  ii} regions (UCH{\sc ii}s, see \citealt{beuther2006b} for a recent
description of the evolutionary sequence)  The first two evolutionary
stages are found within so-called Infrared Dark Clouds (IRDCs)   While
for low-mass stars the chemical evolution from early molecular
freeze-out to more evolved protostellar cores is well studied (e g ,
\citealt{bergin1997,dutrey1997,pavlyuchenkov2006,joergensen2007}),
it is far from clear whether similar evolutionary patterns are present
during massive star formation 

To better understand the chemical evolution of high-mass star-forming
regions we initiated a program to investigate the chemical properties
from IRDCs to UCH{\sc ii}s from an observational and theoretical
perspective  We start with single-dish line surveys toward a large
sample obtaining their basic characteristics, and then perform
detailed studies of selected sources using interferometers on smaller
scales  These observations are accompanied by theoretical modeling of
the chemical processes   Long-term goals are the chemical
characterization of the evolutionary sequence in massive star
formation, the development of chemical clocks, and the identification
of molecules as astrophysical tools to study the physical processes
during different evolutionary stages  Here, we present an initial
study of the reactive radical ethynyl (C$_2$H) combining single-dish
and interferometer observations with chemical modeling   Although
C$_2$H was previously observed in low-mass cores and Photon Dominated
Regions (e g , \citealt{millar1984,jansen1995}), so far it was not
systematically investigated in the framework of high-mass star
formation 

\section{Observations}
\label{obs}

The 21 massive star-forming regions were observed with the Atacama
Pathfinder Experiment (APEX) in the 875\,$\mu$m window in fall 2006 
We observed 1\,GHz from 338 to 339\,GHz and 1\,GHz in the image
sideband from 349 to 350\,GHz   The spectral resolution was
0 1\,km\,s$^{-1}$, but we smoothed the data to
$\sim$0 9\,km\,s$^{-1}$  The average system temperatures were around
200\,K, each source had on-source integration times between 5 and 16
min  The data were converted to main-beam temperatures with forward
and beam efficiencies of 0 97 and 0 73, respectively
\citep{belloche2006}  The average $1\sigma$ rms was 0 4\,K   The main
spectral features of interest are the C$_2$H lines around 349 4\,GHz
with upper level excitation energies $E_u/k$ of 42\,K (line blends of
C$_2$H$(4_{5,5}-3_{4,4})$ \& C$_2$H$(4_{5,4}-3_{4,3})$ at
349 338\,GHz, and C$_2$H$(4_{4,4}-3_{3,3})$ \&
C$_2$H$(4_{4,3}-3_{3,2})$ at 349 399\,GHz)  The beam size was $\sim
18''$ 

The original Submillimeter Array (SMA) C$_2$H data toward the
HMPO\,18089-1732 were first presented in \citet{beuther2005c}  There
we used the compact and extended configurations resulting in good
images for all spectral lines except of C$_2$H  For this project, we
re-worked on these data only using the compact configuration  Because
the C$_2$H emission is distributed on larger scales (see
\S\ref{results}), we were now able to derive a C$_2$H image  The
integration range was from 32 to 35\,km\,s$^{-1}$, and the achieved
$1\sigma$ rms of the C$_2$H image was 450\,mJy\,beam$^{-1}$   For more
details on these observations see \citet{beuther2005c} 

\section{Results}
\label{results}

The sources were selected to cover all evolutionary stages from IRDCs
via HMPOs to UCH{\sc ii}s  We derived our target list from the samples
of \citet{klein2005,fontani2005,hill2005,beltran2006}   Table
\ref{sample} lists the observed sources, their coordinates, distances,
luminosities and a first order classification into the evolutionary
sub-groups IRDCs, HMPOs and UCH{\sc ii}s based on the previously
available data  Although this classification is only based on a
limited set of data, here we are just interested in general
evolutionary trends  Hence, the division into the three main classes
is sufficient 

Figure \ref{spectra} presents sample spectra toward one source of each
evolutionary group  While we see several CH$_3$OH lines as well as
SO$_2$ and H$_2$CS toward some of the HMPOs and UCH{\sc ii}s but not
toward the IRDCs, the surprising result of this comparison is the
presence of the C$_2$H lines around 349 4\,GHz toward all source types
from young IRDCs via the HMPOs to evolved UCH{\sc ii}s   Table
\ref{sample} lists the peak brightness temperatures, the integrated
intensities and the FWHM line-widths of the C$_2$H line blend at
349 399\,GHz  The separation of the two lines of 1 375\,MHz already
corresponds to a line-width of 1 2\,km\,s$^{-1}$  We have three C$_2$H
non-detections (2 IRDCs and 1 HMPO), however, with no clear trend with
respect to the distances or the luminosities (the latter comparison is
only possible for the HMPOs)  While IRDCs are on average colder than
more evolved sources, and have lower brightness temperatures, the
non-detections are more probable due to the relatively low sensitivity
of the short observations (\S\ref{obs})  Hence, the data indicate
that the C$_2$H lines are detected independent of the evolutionary
stage of the sources in contrast to the situation with other
molecules   When comparing the line-widths between the different
sub-groups, one finds only a marginal difference between the IRDCs and
the HMPOs (the average $\Delta v$ of the two groups are 2 8 and
3 1\,km\,s$^{-1}$)   However, the UCH{\sc ii}s exhibit significantly
broader line-widths with an average value of 5 5\,km\,s$^{-1}$ 

Intrigued by this finding, we wanted to understand the C$_2$H spatial
structure during the different evolutionary stages   Therefore, we
went back to a dataset obtained with the Submillimeter Array toward
the hypercompact H{\sc ii} region IRAS\,18089-1732 with a much higher
spatial resolution of $\sim 1''$ \citep{beuther2005c}   Albeit this
hypercompact H{\sc ii} region belongs to the class of HMPOs, it is
already in a relatively evolved stage and has formed a hot core with a
rich molecular spectrum   \citet{beuther2005c} showed the spectral
detection of the C$_2$H lines toward this source, but they did not
present any spatially resolved images  To recover large-scale
structure, we restricted the data to those from the compact SMA
configuration (\S\ref{obs})  With this refinement, we were able to
produce a spatially resolved C$_2$H map of the line blend at
349 338\,GHz with an angular resolution of $2 9''\times 1 4''$
(corresponding to an average linear resolution of 7700\,AU at the
given distance of 3 6\,kpc)  Figure \ref{18089} presents the
integrated C$_2$H emission with a contour overlay of the 860\,$\mu$m
continuum source outlining the position of the massive protostar  In
contrast to almost all other molecular lines that peak along with the
dust continuum \citep{beuther2005c}, the C$_2$H emission surrounds the
continuum peak in a shell-like fashion 

\section{Discussion and Conclusions}

To understand the observations, we conducted a simple chemical
modeling of massive star-forming regions  A 1D cloud model with a mass
of 1200\,M$_\sun$, an outer radius of 0 36\,pc and a power-law density
profile ($\rho\propto r^p$ with $p=-1 5$) is the initially assumed
configuration  Three cases are studied: (1) a cold isothermal cloud
with $T=10$\,K, (2) $T=50$\,K, and (3) a warm model with a temperature
profile $T\propto r^q$ with $q=-0 4$ and a temperature at the outer
radius of 44\,K  The cloud is illuminated by the interstellar UV
radiation field (IRSF, \citealt{draine1978}) and by cosmic ray
particles (CRP)  The ISRF attenuation by single-sized $0 1\mu$m
silicate grains at a given radius is calculated in a plane-parallel
geometry following \citet{vandishoeck1988}  The CRP ionization rate is
assumed to be $1 3\times 10^{-17}$~s$^{-1}$ \citep{spitzer1968}  The
gas-grain chemical model by \citet{vasyunin2008} with the desorption
energies and surface reactions from \citet{garrod2006} is used 
Gas-phase reaction rates are taken from RATE\,06 \citep{woodall2007},
initial abundances, were adopted from the ``low metal'' set of
\citet{lee1998} 

Figure \ref{model} presents the C$_2$H abundances for the three models
at two different time steps: (a) 100\,yr, and (b) in a more evolved
stage after $5\times10^4$\,yr  The C$_2$H abundance is high toward the
core center right from the beginning of the evolution, similar to
previous models (e g , \citealt{millar1985,herbst1986,turner1999}) 
During the evolution, the C$_2$H abundance stays approximately
constant at the outer core edges, whereas it decreases by more than
three orders of magnitude in the center, except for the cold $T=10$~K
model   The C$_2$H abundance profiles for all three models show
similar behavior 

The chemical evolution of ethynyl is determined by relative removal
rates of carbon and oxygen atoms or ions into molecules like CO, OH,
H$_2$O  Light ionized hydrocarbons CH$^+_{\rm n}$ (n=2  5) are quickly
formed by radiative association of C$^+$ with H$_2$ and hydrogen
addition reactions: C$^+$ $\rightarrow$ CH$_2^+$ $\rightarrow$
CH$_3^+$ $\rightarrow$ CH$_5^+$   The protonated methane reacts with
electrons, CO, C, OH, and more complex species at later stage and
forms methane   The CH$_4$ molecules undergo reactive collisions with
C$^+$, producing C$_2$H$_2^+$ and C$_2$H$_3^+$  An alternative way to
produce C$_2$H$_2^+$ is the dissociative recombination of CH$_5^+$
into CH$_3$ followed by reactions with C$^+$   Finally, C$_2$H$_2^+$
and C$_2$H$_3^+$ dissociatively recombine into CH, C$_2$H, and
C$_2$H$_2$  The major removal for C$_2$H is either the direct
neutral-neutral reaction with O that forms CO, or the same reaction
but with heavier carbon chain ions that are formed from C$_2$H by
subsequent insertion of carbon  At later times, depletion and
gas-phase reactions with more complex species may enter into this
cycle   At the cloud edge the interstellar UV radiation
instantaneously dissociates CO despite its self-shielding,
re-enriching the gas with elemental carbon 

The transformation of C$_2$H into CO and other species proceeds
efficiently in dense regions, in particular in the ``warm'' model
where endothermic reactions result in rich molecular complexity of the
gas (see Fig ~\ref{model})   In contrast, in the ``cold'' 10\,K model
gas-grain interactions and surface reactions become important   As a
result, a large fraction of oxygen is locked in water ice that is hard
to desorb ($E_{\rm des} \sim 5500$~K), while half of the elemental
carbon goes to volatile methane ice ($E_{\rm des} \sim 1300$~K)  Upon
CRP heating of dust grains, this leads to much higher gas-phase
abundance of C$_2$H in the cloud core for the cold model compared to
the warm model  The effect is not that strong for less dense regions
at larger radii from the center 

Since the C$_2$H emission is anti-correlated with the dust continuum
emission in the case of IRAS\,18089-1732 (Fig \,\ref{18089}), we do
not have the H$_2$ column densities to quantitatively compare the
abundance profiles of IRAS\,18089-1732 with our model  However, data
and model allow a qualitative comparison of the spatial structures 
Estimating an exact evolutionary time for IRAS\,18089-1732 is hardly
possible, but based on the strong molecular line emission, its high
central gas temperatures and the observed outflow-disk system
\citep{beuther2004a,beuther2004b,beuther2005c}, an approximate age of
$5\times10^4$\,yr appears reasonable   Although dynamical and chemical
times are not necessarily exactly the same, in high-mass star
formation they should not differ to much: Following the models by
\citet{mckee2003} or \citet{krumholz2006b}, the luminosity rises
strongly right from the onset of collapse which can be considered as a
starting point for the chemical evolution  At the same time disks and
outflows evolve, which should hence have similar time-scales   The
diameter of the shell-like C$_2$H structure in IRAS\,18089-1732 is
$\sim 5''$ (Fig \,\ref{18089}), or $\sim$9000\,AU in radius at the
given distance of 3 6\,kpc   This value is well matched by the modeled
region with decreased C$_2$H abundance (Fig \,\ref{model})   Although
in principle optical depths and/or excitation effects could mimic the
C$_2$H morphology, we consider this as unlikely because the other
observed molecules with many different transitions all peak toward the
central submm continuum emission in IRAS\,18089-1732
\citep{beuther2005c}  Since C$_2$H is the only exception in that rich
dataset, chemical effects appear the more plausible explanation 

The fact that we see C$_2$H at the earliest and the later evolutionary
stages can be explained by the reactive nature of C$_2$H: it is
produced quickly early on and gets replenished at the core edges by
the UV photodissociation of CO  The inner ``chemical'' hole observed
toward IRAS\,18089-1732 can be explained by C$_2$H being consumed in
the chemical network forming CO and more complex molecules like larger
carbon-hydrogen complexes and/or depletion 

The data show that C$_2$H is not suited to investigate the central gas
cores in more evolved sources, however, our analysis indicates that
C$_2$H may be a suitable tracer of the earliest stages of (massive)
star formation, like N$_2$H$^+$ or NH$_3$ (e g ,
\citealt{bergin2002,tafalla2004,beuther2005a,pillai2006})  While a
spatial analysis of the line emission will give insights into the
kinematics of the gas and also the evolutionary stage from chemical
models, multiple C$_2$H lines will even allow a temperature
characterization  With its lowest $J=1-0$ transitions around 87\,GHz,
C$_2$H has easily accessible spectral lines in several bands between
the 3\,mm and 850\,$\mu$m   Furthermore, even the 349\,GHz lines
presented here have still relatively low upper level excitation
energies ($E_u/k\sim42$\,K), hence allowing to study cold cores even
at sub-millimeter wavelengths   This prediction can further be proved
via high spectral and spatial resolution observations of different
C$_2$H lines toward young IRDCs 

\acknowledgments{H B  acknowledges financial support
  by the Emmy-Noether-Programm of the Deutsche Forschungsgemeinschaft
  (DFG, grant BE2578)  }



Context 2: Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
https://medical-dictionary thefreedictionary com/Thalassaemia+minor
(redirected from Thalassaemia minor)
Related to Thalassaemia minor: thalassaemia major
Thalassemia describes a group of inherited disorders characterized by reduced or absent amounts of hemoglobin, the oxygen-carrying protein inside the red blood cells  There are two basic groups of thalassemia disorders: alpha thalassemia and beta thalassemia  These conditions cause varying degrees of anemia, which can range from insignificant to life threatening 
All types of thalassemias are considered quantitative diseases of hemoglobin, because the quantity of hemoglobin produced is reduced or absent  Usual adult hemoglobin is made up of three components: alpha globin, beta globin, and heme  Thalassemias are classified according to the globin that is affected, hence the names alpha and beta thalassemia  Although both classes of thalassemia affect the same protein, the alpha and beta thalassemias are distinct diseases that affect the body in different ways 
Beta thalassemia may be the most best-known type of thalassemia and is also called Cooley's anemia  It is caused by a change in the gene for the beta globin component of hemoglobin  Beta thalassemia causes variable anemia that can range from moderate to severe, depending in part on the exact genetic change underlying the disease  Beta thalassemia can be classified based on clinical symptoms  Beta thalassemia major usually causes severe anemia that can occur within months after birth  If left untreated, severe anemia can result in insufficient growth and development, as well as other common physical complications that can lead to a dramatically decreased life-expectancy  Fortunately, in developed countries beta thalassemia is usually identified by screening in the newborn period, before symptoms have developed  Children who are identified early can be started on ongoing blood transfusion therapy as needed  Although transfusion therapy prevents many of the complications of severe anemia, the body is unable to eliminate the excess iron contained in the transfused blood  Over time, the excess iron deposits in tissues and organs, resulting in damage and organ failure  Another medication must be administered to help the body eliminate the excess iron and prevent iron-over-load complications  Beta thalassemia intermedia describes the disease in individuals who have moderate anemia that only requires blood transfusions intermittently, if at all 
Alpha thalassemia is the result of changes in the genes for the alpha globin component of hemoglobin  There are two main types of alpha thalassemia disease: hemoglobin H disease and alpha thalassemia major  The two diseases are quite different from beta thalassemia as well as from one another  Individuals with hemoglobin H disease can experience events of hemolytic anemia—anemia caused by the rapid breakdown of the red blood cells  These events are thought to be triggered by various environmental causes, such as infection and/or exposure to certain chemicals  Hemoglobin H disease is in most cases milder than beta thalassemia  It does not generally require transfusion therapy  Alpha thalassemia major is a very serious disease that results in severe anemia that begins even before birth  Most affected babies do not survive to be born or die shortly after birth 
The thalassemias are among the most common genetic diseases worldwide  Both alpha and beta thalassemia have been described in individuals of almost every ancestry, but the conditions are more common among certain ethnic groups  Unaffected carriers of all types of thalassemia traits do not experience health problems  In fact, the thalassemia trait is protective against malaria, a disease caused by blood-borne parasites transmitted through mosquito bites  According to a widely accepted theory, most genetic changes—mutations—that cause thalassemia occurred multiple generations ago  Coincidentally, these mutations increased the likelihood that carriers would survive malaria infection  Survivors passed the mutation onto their offspring, and the trait became established throughout areas where malaria is common  As populations migrated, so did the thalassemia traits 
Beta thalassemia trait is seen most commonly in people with the following ancestry: Mediterranean (including North African, and particularly Italian and Greek), Middle Eastern, Indian, African, Chinese, and Southeast Asian (including Vietnamese, Laotian, Thai, Singaporean, Filipino, Cambodian, Malaysian, Burmese, and Indonesian)  Alpha-thalassemia trait is seen with increased frequency in the same ethnic groups  However, there are different types of alpha thalassemia traits within these populations  The frequency of hemoglobin H disease and alpha thalassemia major depends on the type of alpha thalassemia trait  The populations in which alpha thalassemia diseases are most common include Southeast Asians and Chinese (particularly Southern Chinese) 
It is difficult to obtain accurate prevalence figures for various types of thalassemia within different populations  This difficulty arises due to testing limitations in determining exact genetic diagnoses, as well as the fact that many studies have focused on small, biased hospital populations 
Two studies reflect prevalence figures that can be helpful counseling families and determining who to screen for beta thalassemia  Between the years of 1990 and 1996, the State of California screened more than 3 1 million infants born in the state for beta thalassemia  Approximately 1 in 114,000 infants had beta thalassemia major, with prevalence rates being highest among Asian Indians (about one in 4,000), Southeast Asians (about one in 10,000), and Middle Easterners (about one in 7,000)  Another type of beta thalassemia disease, E/beta thalassemia, was represented in approximately one in 110,000 births, all of which occurred in families of Southeast Asian ancestry  Among Southeast Asians, the prevalence of E/beta thalassemia was approximately one in 2,600 births  This is in keeping with the observation that hemoglobin E trait carrier rates are relatively high within the Southeast Asian population: 16% in a study of 768 immigrants to California, and up to 25% in some specific Southeast Asian populations such as Cambodians  While these California studies address some of the limitations of earlier population studies, the pattern observed in California is expected to be different in other areas of the United States and the world  For example, Italians are underrepresented in this population when compared to the population of the East Coast of the United States 
Determining prevalence figures for alpha thalassemia is even more difficult due to increased limitations in diagnostic testing  All types of alpha thalassemia disease are most common among people of Southeast Asian and Chinese descent, for reasons that become clearer with an understanding of the underlying genetics of alpha thalassemia  One study of 500 pregnant women in Northern Thailand estimated a frequency of one in 500 pregnancies affected by alpha thalassemia major, for example  Prevalence of alpha thalassemia disease is significantly lower in the United States primarily because of immigration patterns; although at least one state, California, has observed growing hemoglobin H disease incidence rates that are high enough to justify universal newborn screening for the condition 
Humans normally make several types of the oxygen-carrying protein hemoglobin  An individual's stage in development determines whether he or she makes primarily embryonic, fetal, or adult hemoglobins  All types of hemoglobin are made of three components: heme, alpha (or alpha-like) globin, and beta (or beta-like) globin  All types of thalassemia are caused by changes in either the alpha- or beta-globin gene  These changes cause little or no globin to be produced  The thalassemias are, therefore, considered quantitative hemoglobin diseases  All types of thalassemias are recessively inherited, meaning that a genetic change must be inherited from both the mother and the father  The severity of the disease is influenced by the exact thalassemia mutations inherited, as well as other genetic and environmental factors  There are rare exceptions, notably with beta thalassemia, where globin gene mutations exhibit a dominant pattern of inheritance in which only one gene needs to be altered in order to see disease expression  Scientists continue to study the causes  For instance, a new mutation for alpha-thalassemia was discovered for the first time among Iranian patients in 2004 
BETA-THALASSEMIA  Most individuals have two normal copies of the beta globin gene, which is located on chromosome 11 and makes the beta globin component of normal adult hemoglobin, hemoglobin A  There are approximately 100 genetic mutations that have been described that cause beta thalassemia, designated as either beta0 or beta + mutations  No beta globin is produced with a beta0 mutation, and only a small fraction of the normal amount of beta globin is produced with a beta + mutation 
When an individual has one normal beta globin gene and one with a beta thalassemia mutation, he or she is said to carry the beta thalassemia trait  Beta thalassemia trait, like other hemoglobin traits, is protective against malaria infection  Trait status is generally thought not to cause health problems, although some women with beta thalassemia trait may have an increased tendency toward anemia during pregnancy 
When two members of a couple carry the beta thalassemia trait, there is a 25% chance that each of their children will inherit beta thalassemia disease by inheriting two beta thalassemia mutations, one from each parent  The clinical severity of the beta thalassemia disease—whether an individual has beta thalassemia intermedia or beta thalassemia major—will depend largely on whether the mutations inherited are beta0 thalassemia or beta + thalassemia mutations  Two beta0 mutations generally lead to beta thalassemia major, and two beta+ thalassemia mutations generally lead to beta thalassemia intermedia  Inheritance of one beta0 and one beta + thalassemia mutation tends to be less predictable 
Although relatively uncommon, there are other thalassemia-like mutations that can affect the beta globin gene  Hemoglobin E is the result of a substitution of a single nucleotide  This change results in a structurally altered hemoglobin that is produced in decreased amounts  Therefore, hemoglobin E is unique in that it is both a quantitative (i e  thalassemia-like) and qualitative trait  When co-inherited with a beta thalassemia trait, it causes a disease that is almost indistinguishable from beta thalassemia disease  Large deletions around and including the beta globin gene can lead to delta/beta thalassemia or hereditary persistence of fetal hemoglobin (HPFH)  Interestingly, delta/beta thalassemia trait behaves very similarly to beta thalassemia trait in its clinical manifestations  However, HPFH trait does not tend to cause hemoglobin disease when co-inherited with a second thalassemia or other beta globin mutation 
ALPHA-THALASSEMIA  Most individuals have four normal copies of the alpha globin gene, two copies on each chromosome 16  These genes make the alpha globin component of normal adult hemoglobin, which is called hemoglobin A  Alpha globin is also a component of fetal hemoglobin and the other major adult hemoglobin called hemoglobin A2  Mutations of the alpha globin genes are usually deletions of the gene, resulting in absent production of alpha globin  Since there are four genes (instead of the usual two) to consider when looking at alpha globin gene inheritance, there are several alpha globin types that are possible 
Absence of one alpha globin gene leads to a condition known as silent alpha thalassemia trait  This condition causes no health problems and can be detected only by special genetic testing  Alpha thalassemia trait occurs when two alpha globin genes are missing  This can occur in two ways  The genes may be deleted from the same chromosome, causing the 'cis' type of alpha thalassemia trait  Alternately, they may be deleted from different chromosomes, causing the 'trans' type of alpha thalassemia trait  In both instances, there are no associated health problems, although the trait status may be detected by more routine blood screening 
Hemoglobin H disease results from the deletion of three alpha globin genes, such that there is only one functioning gene  Typically, this can occur when one parent carries the silent alpha thalassemia trait, and the other parent carries the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for hemoglobin H disease in each of such a couple's children 
Hemoglobin H disease-like symptoms can also be a part of a unique condition called alpha thalassemia mental retardation syndrome  Alpha thalassemia mental retardation syndrome can be caused by a deletion of a significant amount of chromosome 16, affecting the alpha globin genes  This is usually not inherited, but rather occurs sporadically in the affected individual  Affected individuals have mild hemoglobin H disease, mild-to-moderate mental retardation, and characteristic facial features  This syndrome can also occur as a sex-linked form in which a mutation is inherited in a particular gene on the X-chromosome  This gene influences alpha globin production, as well as various other developmental processes  Individuals affected with this form of the syndrome tend to have more severe mental retardation, delayed development, nearly absent speech, characteristic facial features, and genital-urinary abnormalities  The remaining discussion will focus only on aspects of hemoglobin H disease 
Alpha thalassemia major results from the deletion of all four alpha globin genes, such that there are no functioning alpha globin genes  This can occur when both parents carry the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for alpha thalassemia major in each of such a couple's children 
Beta thalassemia major is characterized by severe anemia that can begin months after birth  In the United States and other developed countries beta thalassemia is identified and treated early and effectively  Therefore, the following discussion of symptoms applies primarily to affected individuals in the past and unfortunately in some underdeveloped countries now  If untreated, beta thalassemia major can lead to severe lethargy, paleness, and delays in growth and development  The body attempts to compensate by producing more blood, which is made inside the bones in the marrow  However, this is ineffective without the needed genetic instructions to make enough functioning hemoglobin  Instead, obvious bone expansion and changes occur that cause characteristic facial and other changes in appearance, as well as increased risk of fractures  Severe anemia taxes other organs in the body—such as the heart, spleen, and liver—which must work harder than usual  This can lead to heart failure, as well as enlargement and other problems of the liver and spleen  When untreated, beta thalassemia major generally results in childhood death, usually due to heart failure  In 2004, the first known heart attack associated with beta thalassemia major was reported  Fortunately, in developed countries diagnosis is usually made early, often before symptoms have begun  This allows for treatment with blood transfusion therapy, which can prevent most of the complications of the severe anemia caused by beta thalassemia major  Individuals with beta thalassemia intermedia have a more moderate anemia that may only require treatment with transfusion intermittently, such as when infections occur and stress the body  As a person with beta thalassemia intermedia gets older, however, the need for blood transfusions may increase to the point that they are required on a regular basis  When this occurs their disease becomes more similar to beta thalassemia major  Other genetic and environmental factors can influence the course of the disease as well  For example, co-inheritance of one or two alpha thalassemia mutations can tend to ameliorate some of the symptoms of beta thalassemia disease, which result in part from an imbalance in the amount of alpha- and beta-globin present in the red blood cells 
Hemoglobin h disease
Absence of three alpha globin genes causes an imbalance of alpha and beta globin proteins in the red blood cells  The excess beta globin proteins tend to come together to form hemoglobin H, which is unable to release oxygen to the tissues  In addition, hemoglobin H tends to precipitate out in the cells, causing damage to the red blood cell membrane  When affected individuals are exposed to certain drugs and chemicals known to make the membrane more fragile, the cells are thought to become vulnerable to breakdown in large numbers, a complication called hemolytic anemia  Fever and infection are also considered to be triggers of hemolytic anemia in hemoglobin H disease  This can result in fatigue, paleness, and a yellow discoloration of the skin and whites of eyes called jaundice  Usually, the anemia is mild enough not to require treatment  Severe anemia events may require blood transfusion, however, and are usually accompanied by such other symptoms as dark feces or urine and abdominal or back pain  These events are uncommon in hemoglobin H disease, although they occur more frequently in a more serious type of hemoglobin H disease called hemoglobin H/Constant Spring disease  Individuals effected with this type of hemoglobin H disease are also more likely to have enlargement of and other problems with the spleen 
Alpha thalassemia major
Because alpha globin is a necessary component of all major hemoglobins and some minor hemoglobins, absence of all functioning alpha globin genes leads to serious medical consequences that begin even before birth  Affected fetuses develop severe anemia as early as the first trimester of pregnancy  The placenta, heart, liver, spleen, and adrenal glands may all become enlarged  Fluid can begin collecting throughout the body as early as the start of the second trimester, causing damage to developing tissues and organs  Growth retardation is also common  Affected fetuses usually miscarry or die shortly after birth  In addition, women carrying affected fetuses are at increased risk of developing complications of pregnancy and delivery  Up to 80% of such women develop toxemia, a disturbance of metabolism that can potentially lead to convulsions and coma  Other maternal complications include premature delivery and increased rates of delivery by cesarean section, as well as hemorrhage after delivery 
Thalassemia may be suspected if an individual shows signs that are suggestive of the disease  In all cases, however, laboratory diagnosis is essential to confirm the exact diagnosis and to allow for the provision of accurate genetic counseling about recurrence risks and testing options for parents and affected individuals  Screening is likewise recommended to determine trait status for individuals of high-risk ethnic groups 
The following tests are used to screen for thalassemia disease and/or trait:
hemoglobin electrophoresis with quantitative hemoglobin A2 and hemoglobin F
free erythrocyte-protoporphyrin (or ferritin or other studies of serum iron levels)
A complete blood count will identify low levels of hemoglobin, small red blood cells, and other red blood cell abnormalities that are characteristic of a thalassemia diagnosis  Since thalassemia trait can sometimes be difficult to distinguish from iron deficiency, tests to evaluate iron levels are important  A hemoglobin electrophoresis is a test that can help identify the types and quantities of hemoglobin made by an individual  This test uses an electric field applied across a slab of gel-like material  Hemoglobins migrate through this gel at various rates and to specific locations, depending on their size, shape, and electrical charge  Isoelectric focusing and high-performance liquid chromatography (HPLC) use similar principles to separate hemoglobins and can be used instead of or in various combinations with hemoglobin electrophoresis to determine the types and quantities of hemoglobin present  Hemoglobin electrophoresis results are usually within the normal range for all types of alpha thalassemia  However, hemoglobin A2 levels and sometimes hemoglobin F levels are elevated when beta thalassemia disease or trait is present  Hemoglobin electrophoresis can also detect structurally abnormal hemoglobins that may be co-inherited with a thalassemia trait to cause thalassemia disease (i e , hemoglobin E) or other types of hemoglobin disease (i e , sickle hemoglobin)  Sometimes DNA testing is needed in addition to the above screening tests  This can be performed to help confirm the diagnosis and establish the exact genetic type of thalassemia 
Diagnosis of thalassemia can occur under various circumstances and at various ages  Several states offer thalassemia screening as part of the usual battery of blood tests done for newborns  This allows for early identification and treatment  Thalassemia can be identified before birth through the use of prenatal diagnosis  Chorionic villus sampling (CVS) can be offered as early as 10 weeks of pregnancy and involves removing a sample of the placenta made by the baby and testing the cells  CVS carries a risk of causing a miscarriage that is between 0 5%-1%  Amniocentesis is generally offered between 15 and 22 weeks of pregnancy, but can sometimes be offered earlier  Two to three tablespoons of the fluid surrounding the baby is removed  This fluid contains fetal cells that can be tested  The risk of miscarriage associated with amniocentesis ranges from 0 33-0 5%  Pregnant woman and couples may choose prenatal testing in order to prepare for the birth of a baby that may have thalassemia  Alternately, knowing the diagnosis during pregnancy allows for the option of pregnancy termination  Preimplantation genetic diagnosis (PGD) is a relatively new technique that involves in-vitro fertilization followed by genetic testing of one cell from each developing embryo  Only the embryos unaffected by sickle cell disease are transferred back into the uterus  PGD is currently available on a research basis only and is relatively expensive 
Individuals with beta thalassemia major receive regular blood transfusions, usually on a monthly basis  This helps prevent severe anemia and allows for more normal growth and development  Transfusion therapy does have limitations, however  Individuals can develop reactions to certain proteins in the blood—called a transfusion reaction  This can make locating appropriately matched donor blood more difficult  Although blood supplies in the United States are very safe, particularly relative to the past and to other areas of the world, there remains an increased risk of exposure to such blood-borne infections as hepatitis  Additionally, the body is not able to get rid of the excess iron that accompanies each transfusion  An additional medication called desferoxamine is administered, usually five nights per week over a period of several hours, using an automatic pump that can be used during sleep or taken anywhere the person goes  This medication is able to bind to the excess iron, which can then be eliminated through urine  If desferoxamine is not used regularly or is unavailable, iron overload can develop and cause tissue damage and organ damage and failure  The heart, liver, and endocrine organs are particularly vulnerable  Desferoxamine itself may rarely produce allergic or toxic side effects, including hearing damage  Signs of desferoxamine toxicity are screened for and generally develop in individuals who overuse the medication when body iron levels are sufficiently low  Overall, however, transfusion and desferoxamine therapy have increased the life expectancy of individuals with the most severe types of beta thalassemia major to the 4th or 5th decade  This can be expected to improve with time and increased developments in treatment, as well as for those with more mild forms of the disease 
New treatments offer additional options for some individuals with beta thalassemia major  There are various medications that target the production of red blood cells (i e  erythropoeitin) or fetal hemoglobin (i e  hydroxyurea and butyrate)  Their effectiveness in ameliorating the severity of beta thalassemia is currently being investigated  Another promising new treatment is bone marrow transplantation, in which the bone marrow of an affected individual is replaced with the bone marrow of an unaffected donor  If successful, this treatment can provide a cure  However, there is an approximately 10-15% chance the procedure could be unsuccessful (i e  the thalassemia returns); result in complications (i e  graft-versus-host disease); or result in death  The risk for specific individuals depends on current health status, age, and other factors  Because of the risks involved and the fact that beta thalassemia is a treatable condition, transplant physicians require a brother or sister donor who has an identically matched tissue type, called HLA type  HLA type refers to the unique set of proteins present on each individual's cells, which allows the immune system to recognize "self" from "foreign " HLA type is genetically determined, so there is a 25% chance for two siblings to be a match  Transplant physicians and researchers are also investigating ways to improve the safety and effectiveness of bone marrow transplantation  Using newborn sibling umbilical cord blood—the blood from the placenta that is otherwise discarded after birth but contains cells that can go on to make bone marrow—seems to provide a safer and perhaps more effective source of donor cells  Donors and recipients may not have to be perfect HLA matches for a successful transplant using cord blood cells  Trials are also underway to determine the effectiveness of "partial transplants," in which a safer transplant procedure is used to replace only a percentage of the affected individual's bone marrow  Other possible treatments on the horizon may include gene therapy techniques aimed at increasing the amount of normal hemoglobin the body is able to make 
Hemoglobin H disease is a relatively mild form of thalassemia that may go unrecognized  It is not generally considered a condition that will reduce one's life expectancy  Education is an important part of managing the health of an individual with hemoglobin H disease  It is important to be able to recognize the signs of severe anemia that require medical attention  It is also important to be aware of the medications, chemicals, and other exposures to avoid due to the theoretical risk they pose of causing a severe anemia event  When severe anemia occurs, it is treated with blood transfusion therapy  For individuals with hemoglobin H disease, this is rarely required  For those with the hemoglobin H/Constant Spring form of the disease, the need for transfusions may be intermittent or ongoing, perhaps on a monthly basis and requiring desferoxamine treatment  Individuals with this more severe form of the disease may also have an increased chance of requiring removal of an enlarged and/or overactive spleen 
Anemia — A blood condition in which the level of hemoglobin or the number of red blood cells falls below normal values  Common symptoms include paleness, fatigue, and shortness of breath 
Bilirubin — A yellow pigment that is the end result of hemoglobin breakdown  This pigment is metabolized in the liver and excreted from the body through the bile  Bloodstream levels are normally low; however, extensive red cell destruction leads to excessive bilirubin formation and jaundice 
Bone marrow — A spongy tissue located in the hollow centers of certain bones, such as the skull and hip bones  Bone marrow is the site of blood cell generation 
Bone marrow transplantation — A medical procedure used to treat some diseases that arise from defective blood cell formation in the bone marrow  Healthy bone marrow is extracted from a donor to replace the marrow in an ailing individual  Proteins on the surface of bone marrow cells must be identical or very closely matched between a donor and the recipient 
Desferoxamine — The primary drug used in iron chelation therapy  It aids in counteracting the life-threatening buildup of iron in the body associated with long-term blood transfusions 
Globin — One of the component protein molecules found in hemoglobin  Normal adult hemoglobin has a pair each of alpha-globin and beta-globin molecules 
Heme — The iron-containing molecule in hemoglobin that serves as the site for oxygen binding 
Hemoglobin — Protein-iron compound in the blood that carries oxygen to the cells and carries carbon dioxide away from the cells 
Hemoglobin A — Normal adult hemoglobin that contains a heme molecule, two alpha-globin molecules, and two beta-globin molecules 
Hemoglobin electrophoresis — A laboratory test that separates molecules based on their size, shape, or electrical charge 
Hepatomegaly — An abnormally large liver 
HLA type — Refers to the unique set of proteins called human leukocyte antigens  These proteins are present on each individual's cell and allow the immune system to recognize 'self' from 'foreign'  HLA type is particularly important in organ and tissue transplantation 
Hydroxyurea — A drug that has been shown to induce production of fetal hemoglobin  Fetal hemoglobin has a pair of gamma-globin molecules in place of the typical beta-globins of adult hemoglobin  Higher-than-normal levels of fetal hemoglobin can ameliorate some of the symptoms of thalassemia 
Iron overload — A side effect of frequent blood transfusions in which the body accumulates abnormally high levels of iron  Iron deposits can form in organs, particularly the heart, and cause life-threatening damage 
Jaundice — Yellowing of the skin or eyes due to excess of bilirubin in the blood 
Mutation — A permanent change in the genetic material that may alter a trait or characteristic of an individual, or manifest as disease, and can be transmitted to offspring 
Placenta — The organ responsible for oxygen and nutrition exchange between a pregnant mother and her developing baby 
Red blood cell — Hemoglobin-containing blood cells that transport oxygen from the lungs to tissues  In the tissues, the red blood cells exchange their oxygen for carbon dioxide, which is brought back to the lungs to be exhaled 
Screening — Process through which carriers of a trait may be identified within a population 
Splenomegaly — Enlargement of the spleen 
Because alpha thalassemia major is most often a condition that is fatal in the prenatal or newborn period, treatment has previously been focused on identifying affected pregnancies in order to provide appropriate management to reduce potential maternal complications  Pregnancy termination provides one form of management  Increased prenatal surveillance and early treatment of maternal complications is an approach that is appropriate for mothers who wish to continue their pregnancy with the knowledge that the baby will most likely not survive  In recent years, there have been a handful of infants with this condition who have survived long-term  Most of these infants received experimental treatment including transfusions before birth, early delivery, and even bone marrow transplantation before birth, although the latter procedure has not yet been successful  For those infants that survive to delivery, there seems to be an increased risk of developmental problems and physical effects, particularly heart and genital malformations  Otherwise, their medical outlook is similar to a child with beta thalassemia major, with the important exception that ongoing, life-long blood transfusions begin right at birth 
As discussed above, the prognosis for individuals with the most serious types of thalassemia has improved drastically in the last several years following recent medical advances in transfusion, chemo-, and transplantation therapy  Advances continue and promise to improve the life expectancy and quality of life further for affected individuals 
"First Known Heart Attack Associated With Beta-thalassemia Major Reported " Heart Disease Weekly February 22, 2004: 10 
"Novel Alpha-thalassemia Mutations Identified " Hematology Week January 26, 2004: 19 
Children's Blood Foundation  333 East 38th St , Room 830, New York, NY 10016-2745  (212) 297-4336  cfg@nyh med cornell edu 
Cooley's Anemia Foundation, Inc  129-09 26th Ave  #203, Flushing, NY 11354  (800) 522-7222 or (718) 321-2873  http://www thalassemia org 
March of Dimes Birth Defects Foundation  1275 Mamaroneck Ave , White Plains, NY 10605  (888) 663-4637  resourcecenter@modimes org  http://www modimes org 
National Heart, Lung, and Blood Institute  PO Box 30105, Bethseda, MD 20824-0105  (301) 592-8573  nhlbiinfo@rover nhlbi nih gov  http://www nhlbi nih gov 
National Organization for Rare Disorders (NORD)  PO Box 8923, New Fairfield, CT 06812-8923  (203) 746-6518 or (800) 999-6673  Fax: (203) 746-6481  http://www rarediseases org 
Bojanowski J  "Alpha Thalassemia Major: The Possibility of Long-Term Survival " Pamphlet from the Northern California Comprehensive Thalassemia Center  (1999) 
Children's Hospital Oakland, Northern California Comprehensive Thalassemia Center website  http://www thalassemia com 
Cooley's Anemia Foundation, Inc  website  http://www thalassemia org/gohome html 
Joint Center for Sickle Cell and Thalassemic Disorders website  http://cancer mgh harvard edu/medOnc/sickle htm 
[thal″ah-se´me-ah]
a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia (alpha-thalassemia) that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia (beta-thalassemia) that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of β-thalassemia, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia; hepatosplenomegaly; skeletal deformation; mongoloid facies; and cardiac enlargement 
thalassemia mi´nor the heterozygous form of β-thalassemia; it is usually asymptomatic, but there may be mild anemia 
sickle cell–thalassemia a hereditary anemia involving simultaneous heterozygosity for hemoglobin S and thalassemia 
thal·as·se·mi·a
, thalassanemia (thal'ă-sē'mē-ă, thă-las-ă-nē'mē-ă),
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia 
[G  thalassa, the sea, + haima, blood]
/thal·as·se·mia/ (thal″ah-se´me-ah) a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of &#x03B2;, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia, hepatosplenomegaly, skeletal deformation, mongoloid facies, and cardiac enlargement 
thalassemia mi´nor the heterozygous form of &#x03B2;, usually asymptomatic, although there is sometimes mild anemia 
(thăl′ə-sē′mē-ə)
An inherited form of anemia occurring chiefly among people of Mediterranean descent, caused by faulty synthesis of part of the hemoglobin molecule  Also called Mediterranean anemia 
thal′as·se′mic adj 
[thal′əsē′mē·ə]
Etymology: Gk, thalassa, sea, a + haima, without blood
production and hemolytic anemia characterized by microcytic, hypochromic red blood cells  Thalassemia is caused by inherited deficiency of alpha- or beta-globin synthesis  See also hemochromatosis, hemosiderosis 
Beta thalassemia, clinical thalassemia, Cooley's anemia, Mediterranean anemia, thalassemia major Hematology A group of genetic diseases by underproduction of hemoglobin due to mutations in the beta globin gene, which is more common in Mediterraneans Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical See Anemia  Cf Sickle cell anemia 
α-thalassemia
Hemoglobin Barts Hematology An inherited condition caused by a defect in the synthesis of the Hb α chain; Hb Barts hemoglobinopathy is characterized by the presence of 4 gamma chains; it is more common in southeast Asians; the most severe form of alpha thalassemia causes stillbirth due to hydrops fetalis Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical Pallor, fatiguability, FTT, fever, infections, diarrhea Management Transfusions
Thalassemia major Hematology A hemoglobinopathy caused by a defect in the synthesis of Hb β chain Clinical Pallor, fatigability, FTT, fever due to infections, diarrhea, bone deformities, hepatosplenomegaly Management Transfusions, but iron overload can damage the heart, liver, and endocrine systems, ergo iron chelation–early use of deferiprone, deferoxamine ↓ transfusion-related iron overload and may protect against DM, cardiac disease, early death
δ-thalassemia
Hematology A condition characterized by a defect of Hb A2–α2δ2; because Hb A2 comprises only 3% of the circulating Hb, even its complete absence; δ-thalassemia has little clinical or hematologic impact
γ-thalassemia
Hematology A condition characterized by a defect of gamma–γ Hb chains found in Hb F–α2γ2; because Hb F is present primarily in the fetus and newborns, it is rarely seen outside of the neonatal period, but may cause transient neonatal hemolytic anemia 
, thalassanemia (thal'ă-sē'mē-ă, -ă-să-nē'mē-ă)
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia  People of Mediterranean, extraction are more often affected than others by this type of anemia 
Synonym(s): thalassaemia, thalassanaemia 
Any of a group of inherited disorders of hemoglobin metabolism with impaired synthesis of one or more polypeptide chains of globin; several genetic types exist 
<a href="https://medical-dictionary thefreedictionary com/Thalassaemia+minor">thalassemia</a>
Barts hemoglobin
beta hemoglobinopathy
beta-delta thalassemia
beta-thalassaemia
Bite Cell
black gallstone
I know of a couple, totally unrelated and unbeknownst to them, who are silent carriers of Thalassaemia minor 
Pakistan: Genetic factor: All in the genes
But, unfortunately, when one person with thalassaemia minor carrier happens to marry another with the same diagnosis, there is a strong possibility that their child would be thalassaemia major, as happened in the case of Taneja 
' My life depends upon a monthly blood transfusion '
0] thalassaemia demonstrates variable severity, ranging from a condition similar to [beta] thalassaemia minor to something approaching thalassaemia major 
A retrospective review of homozygous haemoglobin E patients
Thal, Alan P 
thalame
thalamencephalic
thalamencephalon
thalamic
thalamic fasciculus
thalamic nucleus
thalamic pain syndrome
thalamic peduncle
thalamic radiation
thalamo-
thalamocoele
thalamocortical
thalamocortical fibers
thalamogeniculate artery
thalamolenticular
thalamoperforating artery
thalamostriate radiation
thalamotuberal artery
Thalassaemia minor
thalassaemiaor Cooley's disease
thalassemic facies
thalasso-
Thalassobacter
Thalassobacter utilis
thalassoplankton
thalassoposia
thalidomide neuropathy
Thalidomider
thallium poisoning
Thalarctos
THALAS
Thalasaemia
Thalassaemia Association of Malaysia
thalassaemia major
Thalassaemias
thalassaemic
thalassanaemia
Thalassemia Action Group
Thalassemia Clinical Research Network
thalassemia syndrome
Context 3: Sir Simon William English  (born 30 December 1961) is a New Zealand former National Party politician who served as the 39th prime minister of New Zealand from 2016 to 2017  He had previously served as the 17th deputy prime minister of New Zealand and minister of finance from 2008 to 2016 under John Key and the Fifth National Government 

A farmer and public servant before entering politics, English was elected to the New Zealand Parliament in  as the National Party's candidate in the Wallace electorate  He was elevated to Cabinet in 1996 and in 1999 was made minister of finance, although he served for less than a year due to his party's loss at the 1999 general election  In October 2001, English replaced Jenny Shipley as the leader of the National Party (and consequently as Leader of the Opposition)  He led the party to its worst defeat at the 2002 general election, and as a consequence, in October 2003 he was replaced as leader by Don Brash 

In November 2006, after Brash's resignation, English became deputy leader under John Key  After National's victory at the 2008 general election, he became deputy prime minister and was also made minister of finance for the second time  Under English's direction New Zealand's economy maintained steady growth during National's three terms of government  He became a list-only MP after stepping down as an electorate MP at the 2014 general election 

John Key resigned as leader of the National Party and prime minister in December 2016  English won the resulting leadership election unopposed and was sworn in as prime minister on 12 December 2016  His tenure was only ten months, and included a three-month election campaign  In the 2017 general election, National won the largest number of seats but fell short of a majority  The parties holding the balance of power declined to support the existing government, and English was subsequently replaced as prime minister by Jacinda Ardern, leader of the Labour Party  English initially continued on as Leader of the Opposition, but resigned as leader of the National Party on 27 February 2018 and left parliament two weeks later 

Early life
English was born on 30 December 1961 at Lumsden Maternity Centre in Lumsden  He is the eleventh of twelve children of Mervyn English and Norah (née O'Brien) English  His parents purchased Rosedale, a mixed sheep and cropping farm in Dipton, Southland from Mervyn's uncle, Vincent English, a bachelor, in 1944  English was born in the maternity unit at Lumsden 

English attended St Thomas's School in Winton, then boarded at St  Patrick's College in Upper Hutt, where he became head boy  He played in the first XV of the school's rugby team  English went on to study commerce at the University of Otago, where he was a resident at Selwyn College, and then completed an honours degree in English literature at Victoria University of Wellington 

After finishing his studies, English returned to Dipton and farmed for a few years  From 1987 to 1989, he worked in Wellington as a policy analyst for the New Zealand Treasury, at a time when the free market policies favoured by Labour's finance minister Roger Douglas (known collectively as "Rogernomics") were being implemented 

English joined the National Party in 1980, while at Victoria University  He served for a period as chairman of the Southland branch of the Young Nationals, and became a member of the Wallace electorate committee  After moving to Wellington, he served for periods on the Island Bay and Miramar electorate committees, respectively 

Fourth National Government (1990–1999)

At the 1990 general election, English stood as the National candidate in Wallace, replacing the retiring Derek Angus, and was elected with a large majority  He would hold this seat, renamed Clutha-Southland in 1996, until 2014  He and three other newly elected National MPs (Tony Ryall, Nick Smith, and Roger Sowry) were soon identified as rising stars in New Zealand politics, and at various points were dubbed the "brat pack", the "gang of four", and the "young Turks"  In his first term in parliament, English chaired a select committee into social services  He was made a parliamentary under-secretary in 1993, serving under the Minister of Health 

First period in cabinet (1996–1999)
In early 1996, English was elevated to cabinet by Prime Minister Jim Bolger, becoming the Minister for Crown Health Enterprises and Associate Minister of Education (to Wyatt Creech)  He was 34 at the time, becoming the cabinet's youngest member  After the 1996 general election, the National Party was forced into a coalition with New Zealand First to retain government  In the resulting cabinet reshuffle, English emerged as Minister of Health  However, as a condition of the coalition agreement, NZ First's Neil Kirton (a first-term MP) was made Associate Minister of Health, effectively becoming English's deputy  This arrangement was described in the press as a "shotgun marriage", and there were frequent differences of opinion between the two ministers  After their relationship became unworkable, Kirton was sacked from the role in August 1997, with the agreement of NZ First leader Winston Peters 

As Minister of Health, English was responsible for continuing the reforms to the public health system that National had begun after the 1990 general election  The reforms were unpopular, and health was perceived as one of the government's weaknesses, with the health portfolio consequently being viewed as a challenge  English believed that the unpopularity of the reforms was in part due to a failure in messaging, and encouraged his National colleagues to avoid bureaucratic and money-focused language (such as references to "balance sheets" and "user charges") and instead talk about the improvements to services the government's reforms would bring  He also rejected the idea that public hospitals could be run as commercial enterprises, a view which some of his colleagues had previously promoted 

By early 1997, as dissatisfaction with Bolger's leadership began to grow, English was being touted as a potential successor, along with Jenny Shipley and Doug Graham  His age (35) was viewed as the main impediment to a successful leadership run  National's leadership troubles were resolved in December 1997, when Bolger resigned and Shipley was elected to the leadership unopposed  English had been a supporter of Bolger as leader, but Shipley reappointed him Minister of Health in her new cabinet 

English was promoted to Minister of Finance in a reshuffle in January 1999, a position which was at the time subordinate to the Treasurer, Bill Birch  After a few months, the pair switched positions as part of Birch's transition to retirement, with English assuming the senior portfolio  In early interviews, he emphasised his wish to be seen as a pragmatist rather than an ideologue, and said that the initiatives of some of his predecessors (Roger Douglas's "Rogernomics" and Ruth Richardson's "Ruthanasia") had focused on "fruitless, theoretical debates" when "people just want to see problems solved" 

Opposition (1999–2008)

After the National Party lost the 1999 election to Helen Clark's Labour Party, English continued on in the shadow cabinet as National's spokesperson for finance  He was elected deputy leader of the party in February 2001, following the resignation of Wyatt Creech, with Gerry Brownlee being his unsuccessful opponent



ground_truth: The focus of the study was on the reactive radical ethynyl (C$_2$H).

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What are the symptoms of alpha thalassemia major?

Read the following text and answer briefly.

Context 3: 

Leader of the Opposition
In October 2001, after months of speculation, Jenny Shipley resigned as leader of the National Party after being told she no longer had the support of the party caucus  English was elected as her replacement unopposed (with Roger Sowry as his deputy), and consequently became Leader of the Opposition  However, he did not openly organise against Shipley, and according to The Southland Times "there was almost an element of 'aw, shucks, I'll do it then' about Mr English's ascension" 

Aged 39 when he was elected, English became the second-youngest leader in the National Party's history, after Jim McLay (who was 38 when elected in 1984)  He also became only the third Southlander to lead a major New Zealand political party, after Joseph Ward and Adam Hamilton  However, English failed to improve the party's performance  In the 2002 election, National suffered its worst electoral defeat ever, gaining barely more than twenty percent of the vote  English described it as "the worst day of my political life"  Both party insiders and the general public were split as to how much to blame him for the loss, but most of the party believed that English would be able to rebuild National's support 

By late 2003, however, National's performance in opinion polls remained poor  The party had briefly increased its popularity in the year following the election, but by October its support had fallen to levels only slightly better than what it achieved in the last ballot  English also appeared in a boxing match for a charity against entertainer Ted Clarke  This did not boost his polling or that of the National party either, with suggestions that it devalued his image as a serious politician  Don Brash, former governor of the Reserve Bank and a relative newcomer to politics, began to build up support to replace English  On 28 October, Brash gained sufficient backing in Caucus to defeat English in a leadership contest 

Shadow cabinet roles and deputy leader
On 2 November 2003, when Brash changed responsibilities for certain MPs, English became National's spokesman for education, ranked at fifth place in the party's parliamentary hierarchy  He remained in parliament after the 2005 election  In his new shadow education portfolio, English performed strongly, and remained a party favourite despite his election defeat as leader in 2002, eventually being returned to the finance portfolio in August 2004 as deputy spokesman (while still retaining responsibility for education) 

In November 2006, Brash resigned as leader  English was considered as a potential replacement leader (running against John Key) or deputy leader (against incumbent Gerry Brownlee) in the ensuing leadership election  However, a contest was avoided when the MPs agreed a Key/English ticket would run unopposed in a display of party unity  English took over the deputy leadership and the finance portfolio in the Key shadow cabinet 

Fifth National Government (2008–2017)

Deputy Prime Minister and Minister of Finance (2008–2016)

At the 2008 election, English was re-elected by his electorate, winning by a margin of about 15,500 votes  He became Deputy Prime Minister of New Zealand and Minister of Finance in the fifth National Government, being sworn into office on 19 November 2008 and continued to serve in those roles until becoming Prime Minister on 12 December 2014  He was also made Minister of Infrastructure in National's first term of government and Minister responsible for Housing New Zealand Corporation and minister responsible for the New Zealand flag consideration process in its third 

He was comfortably re-elected in Clutha-Southland in the 2011 election but opted to run as a party-list candidate in 2014  

The pairing of John Key as leader of the National Party and English as his deputy has been compared to that of Bob Hawke and Paul Keating (in Australia) and Tony Blair and Gordon Brown (in the UK) 

English acceded to the role of Finance Minister in the continuing wake of the financial crisis  In response to New Zealand's rising debt, English made budget deficit-reduction his main priority  His first budget outlined three focuses in New Zealand's financial recovery: "improving the business environment and removing roadblocks to growth; investment in productive infrastructure; and improving the way government works"  One of his first acts was creating the National Infrastructure Unit, charged with formulating a plan for infrastructure projects and investments  He commissioned a government-wide spending review, with an aim to reducing government expenditure—with the exceptions of a two-year stimulus package and long-term increases on infrastructure spending 

In April 2011, the Opposition criticised English for suggesting that New Zealand businesses could use New Zealand's low wages to help it compete with Australia  The National Government campaigned for re-election in 2011 on its economic record  The Government boasted growth for five consecutive quarters up to mid-2010, totalling 1 6% of real GDP 

Strong growth resulted in a surplus of $473 million for the 2015/16 financial year, projected to rise to $8 5 billion by 2020/21  In his 2016 Economic and Fiscal Update address, English stated that reducing debt and tackling the costs of the 2016 Kaikōura earthquake were higher priorities than reducing rates of tax 

Allowances issue
In 2009, the media, including TVNZ and TV3 revealed that English was receiving about NZ$900 a week as part of a living allowance for ministers, to live in his own NZ$1 2 million Wellington home  At the time, English also received $276,200 in his annual salary as Deputy Prime Minister  It was also revealed other ministers with homes in the capital city were also claiming accommodation allowances  On 3 August 2009, Prime Minister John Key started a review of the housing allowances claimed by cabinet ministers  English subsequently paid back $12,000 and only claimed about $24,000 a year in living allowances  The Auditor-General's office said in September 2009 that they were making "preliminary enquiries" into parliamentary housing expenses in response to a letter of complaint from Progressive party leader Jim Anderton  Two days later English stated that he would no longer take up any housing allowance and had paid back all the allowance he had received since the November 2008 election 

Prime Minister (2016–2017)

John Key resigned on 12 December, and endorsed English as his successor in the resulting leadership election  Following the drop-out of both Judith Collins and Jonathan Coleman from the leadership election, English was sworn in as the 39th Prime Minister of New Zealand on 12 December 2016 

English appointed his first cabinet on 18 December  In a reshuffle, he appointed Steven Joyce to succeed him as Finance Minister, while most ministerial portfolios remained the same 

In February 2017, English did not attend Waitangi Day commemorations at the historic treaty grounds, reportedly in response to the Ngāpuhi iwi's decision to stop the Prime Minister from speaking at the marae  Ngāpuhi have protested the Government's negotiation of the Trans Pacific Partnership Agreement (TPPA), which the iwi believe infringes upon Māori sovereignty, and thus does not adhere to the Treaty of Waitangi  English had been invited to attend in an official capacity; his non-attendance was criticised by a Ngāpuhi elder and Opposition leader Andrew Little



ground_truth: Severe anemia that begins even before birth.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What position did Simon English hold in the 2008 general election?

Read the following text and answer briefly.

Context 3: 

In his first overseas trip as Prime Minister, English travelled to Europe to discuss trade ties, including a prospective New Zealand–European Union free trade agreement  He first travelled to London on 13 January 2017 to meet British Prime Minister Theresa May  Discussing trade relations, English said the two nations were "natural partners" and would "continue to forge ties" after the UK's withdrawal from the EU  He also arranged to meet with London Mayor Sadiq Khan, Belgian Prime Minister Charles Michel and German Chancellor Angela Merkel   In a meeting with Merkel, English received crucial backing from Germany for a trade deal with the EU  On 16 January, English stated that his government would continue to promote TPPA, despite the United States' decision to withdraw from the agreement  He explained that Southeast Asian countries would now be treated as a priority in negotiations—he also asserted that the United States was ceding influence to China by its rejection of the trade pact 

At a press conference at the Beehive on 1 February 2017, English announced that the 2017 general election would be held on 23 September  The Prime Minister later confirmed that his party would approach ACT, United Future and the Māori Party if confidence and supply agreements were required to form a government following the election  In his second cabinet reshuffle on 24 April, English appointed Gerry Brownlee as his new Foreign Affairs Minister; he also promoted Nikki Kaye to the portfolio of Education Minister, and moved Mark Mitchell into the cabinet to become Defence Minister  The reshuffle was perceived as an election preparation 

On 13 February 2017, English welcomed Australian Prime Minister Malcolm Turnbull to Wellington  The two leaders reaffirmed their shared trade agenda, and discussed changes to the Australian citizenship pathway which will affect permanent residents originating from New Zealand 

On 19 June, it was reported that Todd Barclay, who succeeded English as MP for Clutha-Southland, had clandestinely recorded one of his employee's conversations the previous year, and that John Key's leaders' budget was used to pay a confidential settlement after the employee resigned  English admitted that he had been aware of the illegal recording and the settlement, and thus implicated in the scandal 

During the 2017 National campaign launch, English introduced a $379 million social investment package including digital learning academies for high school students, more resources for mathematics, and boosting support for teaching second languages in schools, and maintaining National Standards in the school curriculum  Prime Minister English also sought to defend National's financial management and economic track record and claimed that the opposition Labour Party would raise taxes  Early opinion polling had forecast a poor showing in the election for the Labour Party, but in early August 37-year-old Jacinda Ardern took over as Labour leader and seemingly energised younger voters 

At the 2017 general election, National won the largest share of the party vote (44 4%) and the largest number of seats (56) in the House Representatives  However, National lacked enough seats to govern alone due to two of the party's support partners, the Māori Party and United Future, losing their parliamentary seats  In response, English stated that the party would be entering into talks to form a coalition with New Zealand First  Following talks with the two largest parties, New Zealand First entered a coalition arrangement with the Labour Party  English was succeeded as prime minister by Jacinda Ardern on 26 October 

Opposition (2017–2018)

Leader of the Opposition
English was re-elected as National Party leader on 24 October 2017  At the time of his re-election, English announced his intention to stay on as leader until the next general election  On 13 February 2018, however, he stood down as National Party leader due to personal reasons, and instructed the party to put into motion the processes to elect a new leader  He also retired from Parliament  English's resignation followed weeks of speculation that he would step aside for a new leader  On 27 February, he was succeeded as party leader by Simon Bridges as the result of the leadership election held that day 

Post-premiership 
In 2018, English joined the board of Australian conglomerate, Wesfarmers  English serves in Chairmanships of Mount Cook Alpine Salmon, Impact Lab Ltd and Manawanui Support Ltd  He is also a director of The Instillery, Centre for Independent Studies and The Todd Corporation Limited, and is a member of the Impact Advisory Group of Macquarie Infrastructure and Real Assets 

Political and social views

English is regarded as more socially conservative than his predecessor, John Key  He has stated his opposition to voluntary euthanasia and physician-assisted suicide, same-sex civil unions, and the decriminalisation of prostitution  As Prime Minister he opposed any "liberalisation" of abortion law 

In 2004, English voted against a bill to establish civil unions for both same-sex and opposite-sex couples  In 2005, he voted for the Marriage (Gender Clarification) Amendment Bill, which would have amended the Marriage Act to define marriage as only between a man and a woman  English voted against the Marriage (Definition of Marriage) Amendment Bill, a bill that legalised same-sex marriage in New Zealand  However, in December 2016 he stated, "I'd probably vote differently now on the gay marriage issue  I don't think that gay marriage is a threat to anyone else's marriage" 

In 2009, English voted against the Misuse of Drugs (Medicinal Cannabis) Amendment Bill, a bill aimed at amending the Misuse of Drugs Act so that cannabis could be used for medical purposes 

Personal life 
English met his future wife, Mary Scanlon, at university  She was studying medicine at the time, and became a general practitioner  Both her parents were immigrants, her father being Samoan and her mother Italian, born on the island of Stromboli  They have six children: a daughter and five sons 

English is a practising Roman Catholic, but has stated that he considers his religious beliefs personal and thus separate from politics 

In June 2002, English took part in TV3's Fight For Life, a celebrity boxing fundraiser to raise money for the Yellow Ribbon anti-youth-suicide campaign, influenced by the death of a teenage nephew in 1997  He lost a split decision to former university colleague Ted Clarke 

Honours
In the 2018 Queen's Birthday Honours, English was appointed a Knight Companion of the New Zealand Order of Merit, for services of over 27 years to the State 

See also

List of New Zealand governments
Politics of New Zealand

References

External links

Profile at National Party 
Profile on Parliament nz
Releases and speeches at Beehive govt nz

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

|-

1961 births
21st-century New Zealand politicians
Candidates in the 2017 New Zealand general election
Deputy Prime Ministers of New Zealand
Leaders of the Opposition (New Zealand)
Living people
Members of the Cabinet of New Zealand
Members of the New Zealand House of Representatives
New Zealand farmers
New Zealand finance ministers
New Zealand list MPs
New Zealand MPs for South Island electorates
New Zealand National Party MPs
New Zealand National Party leaders
New Zealand Roman Catholics
New Zealand people of Irish descent
People educated at St  Patrick's College, Silverstream
People from Dipton, New Zealand
People from Lumsden, New Zealand
Prime Ministers of New Zealand
University of Otago alumni
Victoria University of Wellington alumni
Knights Companion of the New Zealand Order of Merit
New Zealand politicians awarded knighthoods



ground_truth: He became deputy prime minister and minister of finance.