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Clay Sickle

Clay Sickle


Sickle cell disease is challenging but not insurmountable for son of Lakeland commissioner

Lakeland&rsquos Christian Walker has reached a milestone in his 20-year battle with sickle cell disease, an group of inherited red blood cell disorders.

After a blood transfusion this month, he won&rsquot need to keep having transfusions every several weeks.

Ongoing transfusions have been part of the McKeel Academy of Technology graduate&rsquos life since he was a pre-teenager.

Not needing them routinely will be a relief as he juggles studying at Galen College of Nursing in St. Petersburg with working at a Publix store there.

His improvement results from having had transfusions, a change in his medicine, healthy behaviors and determination, mixed with family prayer, to keep the genetic disorder from excessively controlling his life.

&ldquoI was regularly challenged by dealing with sickle cell in daily life,&rdquo he said.

&ldquoBut I was blessed by not having major problems.&rdquo

Christian now is on a drug called hydroxyurea to reduce his need for transfusions and prevent painful crises that can damage organs.

All part of his transition from being treated by the sickle cell team of Johns Hopkins All Children&rsquos Hospital to being with an adult medicine doctor who treats sickle cell patients.

His history of having a silent stroke as a child and other factors specific to his condition led doctors to keep him on blood transfusions until now.

&ldquoHe&rsquos an excellent patient and has been outstanding in his follow up and adherence,&rdquo said Dr. E. Leila Jerome Clay, director of the hospital&rsquos comprehensive sickle-cell program. &ldquoHe would really be a role model for someone to have.&rdquo

Sickle cell symptoms began affecting him as an infant.

His parents, Phillip and Cappie Walker, said the silent stroke occurred sometime in his first years of life. It showed up when routine brain scans started being taken but, fortunately, hadn&rsquot caused any damage.

&ldquoWe learned a lot during our early years,&rdquo said Phillip Walker, a Lakeland city commissioner. &ldquoYou have to research.&rdquo

One of the most important things they learned was Christian&rsquos recurrent risk of going into a sickle cell crisis.

The abnormally shaped red blood cells are in a crescent or sickle shape. That interferes with blood flow and getting oxygen throughout the body.

Anemia and severe chronic inflammation are other dangers of sickle cell disease, which is more common in African Americans, Hispanic-Americans from Central and South America, and people of Middle Eastern, Indian or Mediterranean descent.

About 9,000 Florida residents and about 100,000 nationwide live with it, Clay said.

Christian doesn&rsquot have the most common, severe type, Hbss or sickle-cell anemia, that occurs when a child inherits a sickle cell gene from each parent.

His is a variant called HbS beta thalassemia zero, which means he got a sickle cell gene from one parent and a gene for beta thalassemia (causing anemia) from the other. Beta thalassemia reduces his body&rsquos production of hemoglobin, the protein in red blood cells that spreads oxygen through the body.

So he hasn&rsquot been spared the crises that make sickle cell disease painful and dangerous.

His parents didn&rsquot want him in pain, but they didn&rsquot want him overmedicated. If pain appeared manageable, they preferred treating it first with less-intense drugs and managing the crisis at home.

Preventing a crisis from happening, of course, was even better.

They learned how important it is for him to stay hydrated.

&ldquoSickle cells, if there&rsquos not enough fluid, they will attach to each other, bunch up and cause the pain crisis,&rdquo Cappie Walker said.

They watched for signs of a crisis pending, such as his lips becoming white.

He&rsquos been hospitalized with medical issues an average of a couple of times a year, although less frequently as he got older.

&ldquoAt a young age, it makes you attentive to everything,&rdquo Christian said.

As a little boy, he enjoyed playing basketball at Simpson Park Community Center in Lakeland.

Once regular transfusions began at age 9 or 10, and a port was put in to make those easier, he needed a non-contact sport.

&ldquoWe put him into golf,&rdquo Phillip Walker said. &ldquoHe didn&rsquot like that, of course.&rdquo

&ldquoI wouldn&rsquot say it like that,&rdquo Christian said, noting that he played golf while at McKeel.

&ldquoOther than sickle cell, he was usually a healthy child,&rdquo Cappie Walker said. &ldquoIt&rsquos been a blessing.&rdquo

Initially, he went to Lakeland Regional Medical Center for transfusions but later got them at All Children&rsquos outpatient clinic in Tampa. They started taking him straight to All Children&rsquos Hospital in St. Petersburg, if a crisis occurred, for continuity in his care instead of first getting stabilized at LRMC.

Lakeland Regional&rsquos pediatric emergency department, opened in 2018, now sees &ldquoquite a few&rdquo sickle cell patients. The &ldquovast majority&rdquo can be admitted to LRMC if they need care beyond the emergency department, said Dr. Donna Bhisitkul, medical director of the Children&rsquos Emergency Department.

The addition this year of a pediatric intensive care unit, including a pediatric intensivist, &ldquowill increase our capabilities of caring for these children,&rdquo she said.

Someday Christian may end up treating patients at LRMC himself. He plans to start his health-care career with a two-year nursing degree, then a four-year degree and perhaps continue to become a nurse anesthetist.

He left McKeel in 2018 with a 3.7 grade point average and having earned EKG certification.

His maternal grandparents drew him toward nursing.

William Dennis Cook was a surgical assistant at Duke University initially and then at Watson Clinic and Lakeland. Cappie Christine Cooke was a nurse at Duke and then at LRMC, he said.

&ldquoI think it was mainly because of my grandfather,&rdquo Christian said. &ldquoHe&rsquod get me from school and everything. He used to pick me up and bring me to their house.&rdquo


[note critique]

Benco Nancy L. Manufacture and Use of Clay Sickles from the Uruk Mound, Abu Salabikh, Iraq.. In: Paléorient, 1992, vol. 18, n°1. pp. 119-134.

MANUFACTURE AND USE OF CLAY SICKLES FROM THE URUK MOUND, ABU SALABIKH, IRAQ

Clay sickles are among the most striking ceramic artifacts found at early archeological sites in southern Mesopotamia. These high-fired, sickle- shaped clay objects occur at pre-urban and urban sites on the alluvial plain between the Tigris and Euphrates rivers. They are found concentrated at both large and small settlement sites, as well as scattered across the landscape in areas that might once have been agricultural fields. They appear during the later Ubaid period (ca. 4500-3900 B.C.), continue through the Uruk (ca. 3900-3100 B.C.), and disappear sometime at the beginning of the third millennium.

Despite their widespread distribution and long duration, clay sickles have received surprisingly little concerted attention from archeological researchers. This neglect is partly due to their fragmentary nature and apparent uniformity in shape and paste composition. It also stems from relatively limited excavation at Ubaid and Uruk sites where clay sickles are most common.

The present study attempts to bridge this gap. Based on an examination of clay sickles recovered from the Uruk Mound at Abu Salabikh in southern Iraq, the study aims to : 1) reconstruct the manufacturing technology used in the production of clay sickles, 2) identify variations in clay sickle morphology, and 3) shed some light on the function of clay sickles by examining their spatial distribution at the site and their relationship to other artifact classes.

Previous research on clay sickles

During the last half of the nineteenth century and first half of the twentieth century, Mesopotamian archeologists generally described clay sickles as agricultural tools used for harvesting cereals, possibly as substitutes for flint sickles (1). They viewed clay sickles as part of a broader class of utilitarian ceramic objects, including mullers, hatchets, hammers, and spindle whorls, that had been produced by ancient inhabitants to compensate for their stone-poor but clay-rich environment. Researchers also began to use clay sickles as chronological markers for the Ubaid period in southern Mesopotamia because of their apparent concentration at sites dating to that period (2).

During extensive regional surveys in the 1960s and 1970s, archeologists refined the temporal and spatial distribution of these clay objects (3). The survey data showed that clay sickles made their appearance during the later Ubaid (ca. 4500-

(1) See, for example, HALL 1930 HALL and WOOLLEY, 1927 LLOYD and SAFAR, 1943, 1947, 1948 PARROT, 1948 TAYLOR, 1855 THOMPSON, 1920 WOOLLEY, 1955. (2) LLOYD and SAFAR, 1943 : 155. (3) ADAMS, 1965, 1981 ADAMS and NISSEN, 1972 WRIGHT, 1981.


Presentation of Case

We present the case of a 22-year-old African-American male with hemoglobin SD disease with gram-positive meningitis, sepsis, pneumonia and vaso-occlusive pain crisis after experiencing a headache and fever for 1 week. Lumbar puncture gram stain demonstrated gram-positive cocci in pairs and was treated with meningitic doses of ceftriaxone, vancomycin, and dexamethasone. Four days after admission, his respiratory status progressively worsened with persistent fever and a leukocytosis of >30,000, which led to additional antimicrobial coverage change to piperacillin/tazobactam and meropenem. His CSF cultures from the local hospital grew S. pneumoniae sensitive to vancomycin, ceftriaxone, and penicillin. Four of four blood cultures also from the admitting hospital grew S. pneumoniae sensitive to ceftriaxone, moxifloxacin, penicillin, and vancomycin. Follow-up blood cultures on days 14, 16, and 18 of his illness were negative. The patient was started on prophylactic penicillin at the time of discharge.

His medical history was significant for the diagnosis of sickle cell disease (double heterozygosity for hemoglobins S and D) and asplenia was incidentally noted at eleven years of age. At age 13, he had an episode of multiorgan system failure including severe acute chest syndrome. Additionally, his history included osteomyelitis, avascular necrosis of bilateral femoral heads, and leg ulcers. He had two additional episodes of acute chest syndrome following multiorgan system failure. He was noted to be noncompliant with hydroxyurea. His childhood immunizations were complete. He was last immunized with PPSV23 6 months prior to admission. Prior to this he had received the PPSV23 at ages 7 and 13.

His immunologic evaluation showed elevated IgG (1730 mg/dL) and IgG subclasses, normal IgM and IgA levels. C3 was just below the lower limit of normal (81 and 85 ng/dL with LLN being 88). C4 was normal. IgG responses to diphtheria and tetanus were normal. HIV-1 antigen and antibody and HIV-2 antibody were not found in his serum. His immunoglobin levels for the pneumococcal strains in PPSV23 are shown in Table 1 the initial levels were drawn on hospital day 7. These levels were found to be lower than expected, with eight of the serotypes having levels well below 1.3 μg/mL, which is considered to be the minimum protective level 21 .

Pneumococcal serotype Hospital day 7 4 months posthospitalization 10 months posthospitalization
SEROTYPE 1 4.1 6.2 12.1
SEROTYPE 2 0.6 2.1 6.0
SEROTYPE 3 0.2 1.4 3.6
SEROTYPE 4 2.2 4.6 4.8
SEROTYPE 5 4 6.5 14.1
SEROTYPE 8 2.4 6.6 13.1
SEROTYPE 9N 1.1 3.9 17.0
SEROTYPE 12F 1 1.8 1.7
SEROTYPE 14 3.6 6.6 9.0
SEROTYPE 17F 6.7 19.0 31.6
SEROTYPE 19F 4.2 8.0 8.7
SEROTYPE 20 0.6 3.6 5.1
SEROTYPE 22F 6 31.0 62.4
SEROTYPE 23F 5.8 34.6 83.6
SEROTYPE 6B 2 7.9 29.4
SEROTYPE 10A 2 12.2 24.7
SEROTYPE 11A 1.2 4.0 4.2
SEROTYPE 7F 3.6 17.2 30.9
SEROTYPE 15B 2.6 3.7 3.2
SEROTYPE 18C 0.2 0.6 1.6
SEROTYPE 19A 3.4 7.7 22.8
SEROTYPE 9V 2.7 14.5 27.1
SEROTYPE 33F 0.7 1.8 2.2
  • The patient was immunized with PPSV23 15 years, 9 years and again 7 months prior to the hospitalization, and 2 months posthospitalization. In bold are the levels that are considered to be below the protective level.

Discussion

Spinal cord infarct is infrequent compared to cerebral infarction in the general population, and most commonly occurs as a result of a dissecting aortic aneurysm or aortic surgery [7, 8]. In persons with sickle hemoglobin, significant spinal cord infarction appears to be an even more rare neurologic complication. To the best of our knowledge, there are only two reported cases of other persons, both now deceased, detailing this pathology [4, 5]. Of note, the radiographic findings from our patient have been previously presented in a radiology journal with emphasis on the diffusion-weighted images, but in this report we describe the clinical details and our patient’s subsequent course [6].

There is a case report from 1970 of a 59-year-old Jamaican woman with presumed sickle cell trait who deteriorated over the course of several years to near complete paraplegia and who was subsequently found to have a slightly swollen spinal cord in the cervical region and atrophic thoracic and lumbar spine cord segments on autopsy [4]. The authors noted that her vasculature and neural tissue was otherwise without the stigmata of significant atherosclerotic or degenerative disease, and while no thrombosed vessels were found in relation to the areas of necrosis in her spinal cord, there were however, many arteries and veins distended with abnormally shaped sickle red cells [4]. A 1980 case report describes a 19-year-old African-American man with sickle cell disease who developed sudden-onset quadriplegia and in post-mortem studies was found to have multiple, old, focal and confluent infarcts involving the cortex and subcortical white matter in the brain, and also of the cervical, thoracic, and upper lumbar spinal cord [5]. There are no data from these case reports in the literature concerning other potential risk factors including any thrombophilic abnormalities, as these were not commonly looked for in 1970 and 1980.

From the available reports that have looked for an association between factor V Leiden and complications of sickle cell disease, there is no evidence of an obvious relationship [16, 21, 22]. Kahn et al. studied a cohort of 82 patients with different sickle cell states, 19 of whom had had a stroke [21]. Only one of the 82 was heterozygous for factor V Leiden (there were no homozygotes), and this was not a patient who had experienced a stroke, priapism or any other vascular-type disorder [21]. Andrade et al. similarly examined a cohort of 73 patients with sickle cell disease in Brazil, of whom five had a stroke [16]. One of the five was a heterozygote for factor V Leiden of the patients who had not experienced a stroke, none were positive for the factor V Leiden mutation. Interestingly, that patient had a sister who also had sickle cell anemia and stroke, but the sister did not carry the factor V Leiden mutation. We conclude that our patient’s heterozygosity for factor V Leiden did not contribute to the occurrence of the spinal cord infarction.

Our patient has severe sickle cell disease as manifested by multiple bouts of recurrent acute chest syndrome and the presence of a silent cerebral infarction. As a comorbidity which predisposes to more severe disease, he also has asthma. However, he would not be considered to be very unusual in having this degree of illness. Therefore, the question arises as to why he developed the rare complication of spinal cord infarction. It occurred during the recovery from an episode of acute chest syndrome, which is known to be a time period of increased risk for cerebral infarction, but this is clearly not a full explanation given the frequency of acute chest syndrome and the rarity of spinal cord infarction. His hypoxemia had resolved when the spinal cord infarction occurred, and his worsened anemia had been corrected. In addition, his sickle hemoglobin percentage was quite low. Although our review of the literature does not suggest that his infarct can be explained by the factor V Leiden heterozygosity, he was not tested for any of the other genetic variants that have been recently found to be associated with stroke in SCD such as ANXA2, TGFBR3, and TEK. It is possible that a combination of factor V Leiden heterozygosity and another mutation may increase his risk for this complication. However, in order to determine risk factors for this complication, its true incidence in SCD must be known.


4 RESULTS

4.1 Demographic variables

Table 1 shows the detailed results on the socio-demographic variables. The findings demonstrated a trend consistent with the broad academic literature (Al Nagshabandi & Abdulmutalib, 2019 Blake et al., 2018 Matthie et al., 2015 ). There were more women participants (65%), most respondents lived with family/friends (72%), per cent single (55%), most had secondary level education and the mean hospital emergency visits yearly was 3 (the same as found by Matthie et al., 2015 ). A notable finding from this study was that most SCD patients held full-time jobs (58.8%), while 13% had part-time jobs.

Variable Freq. (N) %
Gender
Female 55 64.7
Male 30 35.5
Education
Primary/JHS 16 18.8
Secondary/SHS 39 45.9
Diploma non-degree 10 11.8
Bachelor degree 15 17.6
Master's degree 5 5.9
Employment
Full-time 50 58.8
Part-time 11 12.9
Unemployed 24 28.2
Marital status
Single 47 55
Married 29 34.5
Divorced/separated 9 10.5
Living situation
Living alone 23 27
Shared housing with family 59 69.4
Shared housing with friends 2 2.6
Variable (Scale) Mean Stand. Dev.
Respondent's age 30 (Max = 53 Min = 18) 7.81
Emergency hospital visits yearly 3 (Max = 12 Min = 1) 1.64
Age at first SCD diagnosis 8.24 (Max = 34 Min = 1) 4.97

4.2 Correlation analysis

4.2.1 Self-efficacy

The correlation results showed a low positive and significant correlation between self-efficacy and self-management (r = 0.357, p < .01), a significant moderate negative relationship between self-efficacy and uncertainty (r = −0.459, p < .01), also, a significant low and positive correlation between self-efficacy and living situation (r = 0.327, p < .01).

4.2.2 Self-management

The results showed a significant low negative relationship between self-management and uncertainty (r = −0.260, p < .05). The correlations between self-management, number of emergency hospital visits in a year and living situations were insignificant.

Furthermore, the correlation between uncertainty and living situation was significant low and negative (r = −0.312, p < .01). But there was an insignificant correlation between uncertainty and number of emergency hospital visits in a year. The significant results from correlation analysis are presented in Table 2.

Efficacy Self-care Uncertainty Emergency visits Living situation
Self-efficacy 1 0.357 a a Correlation is significant at the .01 level.
−0.459 a a Correlation is significant at the .01 level.
0.327 a a Correlation is significant at the .01 level.
Self-care 1 −0.260 b b Correlation is significant at the .05 level.
Uncertainty 1 −0.312 a a Correlation is significant at the .01 level.
  • a Correlation is significant at the .01 level.
  • b Correlation is significant at the .05 level.

4.3 Multiple regression analyses

The second objective of study was analysed using the multiple regression equation. Overall three regression models were employed with self-management, uncertainty and self-efficacy as dependent variables, while the socio-demographics served as explanatory variables. The findings are shown in Tables 3–5.

Variables B SE SB T p
Constant 86.291 2.150 40.131 .001
Employment 1.603 0.513 0.363 3.123 .003
Marital status 1.907 0.585 0.353 3.261 .002
Gender −1.853 0.885 −0.231 −2.094 .040
Living situation −0.840 806 −0.107 −1.042 .301
Variables B SE SB T p
Constant 84.754 6.332 13.385 .001
Years of sch. 2.733 1.369 0.266 1.997 .050
Gender 6.104 2.748 0.263 2.221 .030
Living sitn. −6.139 2.545 −0.269 −2.412 .018
Employment −0.211 1.667 −0.017 −0.127 .900
Variables B SE SB T p
Constant 31.688 1.720 18.428 .001
Gender −1.993 0.764 −0.323 −2.610 .011
Living sitn. 1.308 0.691 0.215 1.893 .062
Years of sch. 0.603 0.326 0.221 1.849 .069

4.3.1 Model 1: Self-management as dependent variable

The predictors were employment, marital status, living situation and gender. The model accounted for 33% of variance in self-management and was statistically significant (R-square = 0.331 F(4, 70) = 8.64, p < .01). Both the techniques of stepwise regression and forced entry were used to examine relationships. Employment, marital status and gender significantly predicted self-management.

4.3.2 Model 2: Uncertainty as dependent variable

The predictors included employment, marital status, education, gender and living situation. The independent variables collectively accounted for 28.4% of variance in uncertainty and was statistically significant (R-square = 0.284 F(4, 71) = 7.036, p < .01). Living situation and education significantly predicted uncertainty in illness.

4.3.3 Model 3: Self-efficacy as dependent variable

The explanatory variables were living situation, education and gender. The predictors collectively explained 19% of variance in self-efficacy and the model was statistically significant (R-square = 0.190 F(3, 72) = 5.63, p < .01). Education (p = .069) and living situation (p = .062) did not predict self-efficacy.


Examples of U.S. Trade Enhancement Programs

  • 1938: The U.S. government price-support program, the Commodity Credit Corporation, was formed.
  • 1949: The International Wheat Agreement specifies quantities of wheat that could be sold abroad at a fixed range of prices.
  • 1954: Agricultural Trade Development and Assistance Act or Public Law 480 allowed the U.S. government to make agreements for wheat sales or barter.
  • 1959: Public Law 480 was amended to include long-term agreements and credit extensions for sales of surplus farm products.
  • 1990: Export Enhancement Program (EEP) created.

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When the Committee met last autumn to make a decision on the Society&rsquos next local exhibition the excavations at Bellfield were suggested. All signs of the dig and finds by Headland Archaeology, although recorded, had been covered over and built on, a street sign the only local clue that prehistoric remains had been uncovered. How could we develop an interesting project that would involve the community? A chance meeting solved the problem and led to a series of community events and activities which would reveal the life and work of the Bronze Age community that lived in Bellfield nearly 3,000 years ago.

We needed expert help and it was decided to apply for Heritage Lottery Funding along with grants from Highland Council Ward Discretionary Fund and STEMNet to make it possible. The Society is very grateful that these agencies felt they could support our year long project.


Feats of Clay: an investigation into the Bronze Age in the North Kessock Area can now go ahead.

Based on the finds at Bellfield and the important part clay played in the domestic ware, house building and metal working of the time, this project offers a series of field activities, community courses, a Crafting Day during Highland Archaeology Festival in October where members of the public will be able to engage with Bronze Age (BA) Crafts and witness the casting of a replica BA sickle.

Only 5 of these socketed sickles have been found in Scotland but North Kessock revealed BA clay moulds for casting these tools, the only such evidence to be found in Britain. The expert-led project will continue with talks, visits to schools and the National Museum and will be brought to a close with our 6th Exhibition in September 2014 when a publication recording the entire project will be launched. Trevor Cowie of National Museums of Scotland has volunteered to write the text using photos taken by members of the community.

Possible Sources of Clay: In trying to identify sources of clay, we talked to local people, especially farmers and local historians. They were able to direct us to several potential sites. We then held four group sessions. The first, to share 'intelligence' of all the identified sites and select the best options. The second to visit the Highland Archives to scrutinise old maps of these potential sites for indications of suggestive place names and for clay holes or pits. Finally, we held two clay hunting days during which we collected samples from the most likely sources.


Clay Sickle - History

Manners & Customs : Sickles

Sickle in Easton's Bible Dictionaryy of the Egyptians resembled that in modern use. The ears of corn were cut with it near the top of the straw. There was also a sickle used for warlike purposes, more correctly, however, called a pruning-hook (Deut. 16:9 Jer. 50:16, marg., "scythe" Joel 3:13 Mark 4:29).

Sickle in Naves Topical Bible An agricultural implement used for cutting grain De 23:25 Jer 50:16 Mr 4:29 -FIGURATIVE Of the judgments of God Joe 3:13 Re 14:14-19

Sickle in the Bible Encyclopedia - ISBE sik'-'l (chermesh (Dt 16:9 23:25), maggal compare Arabic minjal (Jer 50:16 Joel 3:13) drepanon (Mk 4:29 Rev 14:14- 19)): Although the ancients pulled much of their grain by hand, we know that they also used sickles. The form of this instrument varied, as is evidenced by the Egyptian sculptures. The earliest sickle was probably of wood, shaped like the modern scythe, although much smaller, with the cutting edge made of sharp flints set into the wood. Sickle flints were found at Tel el-Chesy. Crescent-shaped iron sickles were found in the same mound. In Israel and Syria the sickle varies in size. It is usually made wholly of iron or steel and shaped much like the instrument used in western lands. The smaller- sized sickles are used both for pruning and for reaping.

Sickle Scripture - Deuteronomy 16:9 Seven weeks shalt thou number unto thee: begin to number the seven weeks from [such time as] thou beginnest [to put] the sickle to the corn.

Sickle Scripture - Deuteronomy 23:25 When thou comest into the standing corn of thy neighbour, then thou mayest pluck the ears with thine hand but thou shalt not move a sickle unto thy neighbour's standing corn.

Sickle Scripture - Jeremiah 50:16 Cut off the sower from Babylon, and him that handleth the sickle in the time of harvest: for fear of the oppressing sword they shall turn every one to his people, and they shall flee every one to his own land.

Sickle Scripture - Joel 3:13 Put ye in the sickle, for the harvest is ripe: come, get you down for the press is full, the fats overflow for their wickedness [is] great.

Sickle Scripture - Mark 4:29 But when the fruit is brought forth, immediately he putteth in the sickle, because the harvest is come.

Sickle Scripture - Revelation 14:14 And I looked, and behold a white cloud, and upon the cloud [one] sat like unto the Son of man, having on his head a golden crown, and in his hand a sharp sickle.

Sickle Scripture - Revelation 14:15 And another angel came out of the temple, crying with a loud voice to him that sat on the cloud, Thrust in thy sickle, and reap: for the time is come for thee to reap for the harvest of the earth is ripe.

Sickle Scripture - Revelation 14:16 And he that sat on the cloud thrust in his sickle on the earth and the earth was reaped.

Sickle Scripture - Revelation 14:17 And another angel came out of the temple which is in heaven, he also having a sharp sickle.

Sickle Scripture - Revelation 14:18 And another angel came out from the altar, which had power over fire and cried with a loud cry to him that had the sharp sickle, saying, Thrust in thy sharp sickle, and gather the clusters of the vine of the earth for her grapes are fully ripe.

Sickle Scripture - Revelation 14:19 And the angel thrust in his sickle into the earth, and gathered the vine of the earth, and cast [it] into the great winepress of the wrath of God.

Tares Tares. The tares are also enemies of the grain. In his Parable of the Tares, JESUS said: "While men slept, his enemy came and sowed tares among the wheat" (Matthew 13:25). In the Holy Land, tares are something called "wild wheat," because they resemble wheat, only the grains are black. Thomson has this to say about the tares: "The Arabic name for tares is zawan, and they abound all over the East, and are a great nuisance to the farmer. The grain is small, and is arranged along the upper part of the stalk, which stands perfectly erect. Its taste is bitter, and when eaten separately, or when diffused in ordinary bread, it causes dizziness, and often acts as an emetic. In short, it is a strong soporific poison, and must be carefully winnowed, and picked out of the wheat, grain by grain, before grinding, or the flour is not healthy. Of course the farmers are very anxious to exterminate it, but that is nearly impossible. [Manners And Customs of Bible Lands]

The Sickle CUTTING AND TRANSPORTING THE RIPENED GRAIN Cutting the ripened grain. The ripe grain is cut with a sickle. In early times sickles were made of flint, which material was abundant and therefore cheap. In later periods there were some made of bronze or of iron, but the former were more prevalent in all periods. The flint was at first set in the jaw-bone of an animal, or in a curved piece of wood. The prophet Jeremiah speaks of "him that handleth the sickle in the time of harvest" (Jeremiah 50:16). And the prophet Joel commands: "Put ye in the sickle, for the harvest is ripe" (Joel 3:13). [Manners And Customs of Bible Lands]


How is the hemoglobin S gene inherited?

When the hemoglobin S gene is inherited from only one parent, and a normal hemoglobin gene—hemoglobin A—is inherited from the other, that person will have sickle cell trait. People who have sickle cell trait are generally healthy.

Only rarely do people who have sickle cell trait have complications similar to those seen in people who have sickle cell disease. But people who have sickle cell trait are carriers of a defective hemoglobin S gene, so they can pass it on when they have a child.

If the child’s other parent also has sickle cell trait or another abnormal hemoglobin gene, such as beta- thalassemia , hemoglobin C, hemoglobin D, or hemoglobin E, that child has a chance of having sickle cell disease.

Inheritance pattern for sickle cell disease. The image shows how hemoglobin S genes are inherited. A person inherits two hemoglobin genes—one from each parent. A normal hemoglobin A gene will make normal hemoglobin. A hemoglobin S gene will make abnormal hemoglobin.

In the image above, each parent has one normal hemoglobin A gene and one hemoglobin S gene, which means each of their children has:

  • A 25% chance of inheriting two normal hemoglobin A genes. In this case, the child does not have sickle cell trait or disease.
  • A 50% chance of inheriting one normal hemoglobin A gene and one hemoglobin S gene. This child has sickle cell trait.
  • A 25% chance of inheriting two hemoglobin S genes. This child has sickle cell disease.

It is important to keep in mind that each time this couple has a child, the chances of that child having sickle cell disease remain the same. In other words, if the firstborn child has sickle cell disease, there is still a 25% chance that the second child will also have the disease. Both boys and girls can inherit sickle cell trait, sickle cell disease, or normal hemoglobin.

If a person wants to know whether he or she carries a sickle hemoglobin gene, a doctor can order a blood test to find out.


Watch the video: Rubys Scythe - Polymer Clay Tutorial Mobile Legends Bang Bang (December 2021).