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How can I find a real software project data sets for validating an early software reliability prediction model?

Question

Sep 2015

I'm working on my thesis that's about early software reliability prediction using reliability relevant metrics in requirement , design and code phase by the use of fuzzy logic.

i need a data set in order to evaluate my proposed three level fuzzy model.

the metric that I'm going to use,are : requirement change request,requirement fault density,review inspection and walkthrough (in requirement phase);cyclomatic complexity,design defect density,fault density (in design phase);program capability and process maturity ( in code phase).

i need numerical value for each metrics in dataset.

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5 Answers

What is your take on future solar PV technologies?

Question

Apr 2016

In the context of the Low Carbon Energy Observatory of the Joint Research Centre we are opening up a consultation in order to identify which are the more promising emerging solar photovoltaic (PV) technologies.

(How to define emerging solar PV technologies? These are technologies still far away from the maturity, with a TRL of 1-4, still researched at the university level, rather than in big companies.)

I would like to have your views on what you consider the most interesting emerging solar PV technologies, in the medium-long term.

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What kind of systematic inputs or triggers are needed for a knowledge building community or class?

Question

Sep 2014

From the perspective of systems thinking, we can view a classroom as a system: composed of dynamic units or actors, autonomous, and part of a larger system. A system also gets inputs. For an actively engaged and knowledge building classroom, what initial inputs or preparation is necessary? In addition to a certain level of maturity and prior knowledge, does this system require some initial "knowledge transfer" from a teacher, mentor, or supervisor? What form does this come in (e.g. establishing rules, providing effective reading or learning tips, teaching a certain amount of background theory, and so on)? What do you think? Any concrete examples of initial preparation, inputs, or direct transfers in your face-to-face or online classes, or at the institutions you have studied or worked in, that helped achieve heutagogy and knowledge building?

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Does applying edible coating on Cavendish banana Risk of no peel color change to yellow?

Question

Jun 2022

Hello, previously I've tried to apply edible coating (chitosan-based) on cavendish banana with maturation level on stage 3. However, a problem occurs in the color of the banana peel that does not change to yellow while the pulp is getting softer and sweeter (green soft). I also tried to coat the banana in stages 4-5 which resulted in it brown spot that spread evenly through the peel surface. I planned to repeat the observation in stage 1 cavendish banana but I am still worried that the problem occurs again. In addition, most of the journals use stage 1 cavendish banana and it shows the color successfully changes.

What factors that cause cavendish banana peel color doesn't change? Does maturity level need to be considered while applying the edible coating in order to achieve an acceptable quality of coated bananas?

ps: the banana is already treated with ethylene to induce the ripening & color change before the coating is applied.

Anyone who is experienced in this, please kindly answer my question, I really need to find the solution. Thank you!:)

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How to identify/measure to what extent a project applied a co-creational approach?

Question

Jan 2018

Co-creation is based on a few basic principles. However, now I want to test projectteams to what extent they have met a co-creational approach.

Therefore i'm looking for indicators who can tell something about the level of maturity of applying a co-creational approach.

For example: A meeting is conducted with all stakeholders (inc. end users) in which a brainstorm was organized.

Or: A platform (offline or online) was provided in which stakholders could react on each other.

At best i'm hoping to find some indicators for each principle:

Dialogue, Access, Risk Reduction, Transparancy (Prahalad & Ramaswamy) and Equality among stakeholders.

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Would you consider sharing the full paper?

Question

Nov 2019

The economics of governance and the impact of strategies on the economics of living is well understood but very poorly practiced. Hence the paper is well timed and its impact on the purposeful governance to create value for the public at large is very high. Welcome to the initiative.

The question arises the creation of meaningful utilization of the resources available in abundance: to what extent all the resources available are put to use. If an analysis is made of the resources we are blessed with in terms of the demographic distribution, it can be found a large percentage of resources forming the age group above sixty is never put to use despite the fact that they are the resources most blessed with the wisdom of application in terms of experience, maturity and expertise and availability. This is at a time we are weeping of the shortage of the right talent to meet a given situation at a cost manageable. Is this aspect of the economics of resources dealt at length in the paper.

How do you propose the retirement age of the day in a context the longevity is increasing from a level of 60 or so to as high as 70: the period of life fit enough for a useful service

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How intelligent are current ERP systems ?

Question

Nov 2021

Hello everyone,

As many of you are aware, Industry 4.0 and smart manufacturing is widely gaining traction among many manufacturing practitioners.

One of the aims of smart manufacturing is to bring in more real-time intelligence to shop-floor and manufacturing planners, by employing different shop-floor data sources (For eg, smart products, advanced equipment and machine sensors, collated through the Industrial Internet of things, RFID gateways, etc). The data collected from these shop-floor data sources can be processed by means of Artificial intelligence-based algorithms ( machine learning, evolutionary algorithms, etc) to produce optimized production schedules, process plans, service schedules, and maintenance plans. The application of such techniques has been researched by several researchers and numerous publications are already available.

However, at the same time, central to the functioning of any manufacturing industry are Manufacturing resource planning software packages, which over the last two decades have transformed into Enterprise resources planning packages, encompassing all the functions of a manufacturing business, ranging from procurement to production planning and control to service management and even auxiliary support functions such as accounting and packages.

As a result, there are two different software systems that can benefit manufacturing firms:

1. AI-based smart manufacturing tools which seem promising in improving production efficiency

2. Tried and tested ERP work packages, developed by numerous software firms.

The question that I often wonder about is : Have AI- algorithm based smart manufacturing tools been integrated into existing ERP softwares?

What is the level of maturity of ERP work packages with respect to AI-based intelligence algorithms?

Many ERP work packages support multiple scheduling rules for a host of production scenarios such as flow manufacturing, make to stock, make to order, job shop- etc.

But do they actually employ AI Solvers- such as genetic algorithms, search-based algorithms, Neural network models, reinforcement learning-based algorithms?

Is the development in these two work packages progressing in two nonintersecting planes ?

I've found a few articles on Intelligent ERP systems, but they are pretty generic, and mainly focus on the need for ERP systems to integrate cloud and mobile based support and automated inspections, but do not touch upon AI sovlers.

A search on google scholar does not reveal much either.

Looking forward to your valuable answers!

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NASA Office of Chief Technologist (OCT)

Question

Apr 2011

NASA

industry.

Performing these flight demonstrations is intended to advance the readiness of the selected systems, provide tangible products capable of rapid infusion to NASA missions, and capture significant public interest and awareness. Furthermore, executing these engaging and technically challenging space flight demonstrations, including designing the flight test program, building the flight hardware and performing/operating the flight demonstration is an outstanding means for developing the current NASA and industry workforce to handle more challenging and more sustainable space missions and operations in the future.

Technical risk, technology maturity, mission risk, customer interest, and proposed cost are discriminators used in the selection process. For infusion purposes, NASA-industry teams are required to have a sponsor (or sponsors) willing to cost share a minimum of 25% of the proposed development effort. Total Office of Chief Technologist (OCT) funding for a capability demonstration mission under the TDM Program may range from $10 million to approximately $150 million. In rare cases, Life Cycle Costs greater than $150 million may be considered by OCT if the proposed effort presents a compelling new technological capability and warrants a higher funding level. Costs include all elements of the flight test demonstration including test planning, flight hardware, launch costs, ground operations, and post testing assessment/ reporting. In addition to the above criteria, for selection as a Crosscutting Capability Demonstration project, the candidate technology must be relatively mature (TRL of 4 or above), and if successful must raise the TRL of the candidate technology to a TRL of 6 or higher, such that it may be infused into the critical path for future NASA missions, or demonstrate a significant new industry capability. Competed flight test demonstration opportunities are open to teams involving NASA centers, industry, other Government agencies and academia. TDM projects will be governed by tailored versions of NPR 7120.5D (Space Flight Programs/Projects); tailoring is encouraged for projects.

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What are the concepts and rationales for designing transgenic organisms consisting of exclusively sexually reproducing cells?

Question

Apr 2018

What are the concepts and rationales for designing transgenic organisms consisting of exclusively sexually reproducing cells as necessary foundation for increasing longevity and reducing carcinogenesis?

I am assuming that the antagonistic nature of reactivating telomerase to allow indefinite cell division and getting one more mutation to cancer and the problem caused when trying to replicate the telomere ends are well understood. If not, I am happy to explain and elaborate.

Are cancer prevention and immortality mutually exclusive? Who wouldn't like to be almost completely immune to cancer and at the same time live forever? But how to unify these objectives which seem to be mutually exclusive at a first glance? The rationale for the assumed exclusivity of these two objectives is shown in the picture below:

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Why can't we pass on our genes for only 120 years to our progeny somatic cells? How can we accumulate so many mutations within our short lifespan that we cannot live beyond 120 years? Is it impossible to live any longer than that? Is aging programmed or accidental? How is it possible that we - as a species called Homo sapiens - have passed on our genes very successfully and have even become better adapted to our environment without suffering from any genetic deterioration whereas our somatic genes are deteriorating very rapidly from the time we were conceived? On a somatic (individual) and species level, we are passing on our genes through cell division. Why is it working so much better on a species than on a somatic level? If we could find out the cause, maybe we could apply this difference in gene transmission mechanism to transfer the apparent advantages from the species level down to the organism level.

There must be a way because it is already working. We might better understand if we could only imagine, i.e. think of each cell as a person and the entire organism as a species. If we could make our cells behave and replicate like individual humans - then - we should benefit from the same underlying mechanism that is currently only acting on a species level but not yet on the level of each individual organism. But does this necessarily mean that it cannot happen anytime soon? The odds to transfer the species replication advantage down to the level of individual people are rising exponentially as soon as we know what we are shooting for, no matter how crazy it looks at a first glance.

I am just feeling very strongly that people are neglecting to worry about their individual survival until they are about to die and when it is obviously way too late for actively contributing towards extending their lifespan. I'd like to compare this lack of insight to somebody, who is never backing up his hard drive, despite being completely aware that it will fail one day for sure.

I am a very compassionate writer. I lost most of my writings in a hard drive crash in April of 2011 at the Lion's World Services for the Blind because my black 2.5 inch Passport USB hard drive, which I have been using for backups, crashed only a few days after my laptop hard drive crashed; thus not giving me enough time to buy another backup hard drive. For a long time I felt almost as if I had died because all my writings, which I believe define - at least to some extent - who I am today, have been irreversibly lost. I sent both of my hard drives to 3 different data recovering companies but none of them could restore my data, not even the directory where I had saved my most favorite writings, which I intended to improve as soon as time, energy and circumstances would permit.

Now however, after loosing almost everything, I have to start from scratch but I believe I'd never be able to restore all my thoughts, which I believed to have securely and permanently saved on both of my now broken hard drives. Then what is the value of all his work when considered from the perspective of any time point after his hard drive has crashed and permanently failed. Since, who we are as an individual person is exclusively defined by our experiences and their interpretation, the end of our lives, which is preventing us from making and responding to new experiences is very similar to a crashing hard drive inevitably rendering all saved information meaningless.

Has humanity as a whole ever suffered from something similar to cancer? Are we experiencing as many replication errors when having children than we do when our somatic cells divide? The answer is an emphatic NOOOOOOO!!!!!! But why not?

Maybe it’s not as clear cut as I just thought. Maybe people, who are not contributing to society, who are committing crimes and must be put to jail, are harming the society since imprisonment is at least as expensive as the finest education at our best universities. When stretching it a little bit, we can compare criminals with cancerous tumors because both are harming the living entity that is composed of them, whether its homo sapiens or me. But wouldn't we all tend to become like cancer cells, if we had no measures to force everyone to contribute by paying taxes for example if we wouldn't have to? Would we get up to work everyday, if we'd even get paid regardless whether or not we are doing our job? Again - NOO!

But, what about cancer cells? Who or what is forcing them to keep contributing to our body rather than replicating on its expense thus harming it until it dies, which is ending the life of the tumor soon after too. Therefore, we must find ways to force our cells to keep contributing and to only permit contributing cells to replicate and to positively select for those cells who are improving their overall contribution? How can this ever be done? Should we consider paying our cells? She we restrict ATP only to those cells that are contributing and let the cancer cells starve by depriving them of ATP? This would be one possibility. But how to prevent cancer cells from making ATP?

We can either think of a human like a species consisting of many highly specialized groups of citizens. Then our cerebrum neurons would represent researchers, professors, and decision makers. Our kidneys would represent custodians. The liver would stand for those involved in cleaning up the environment, or red blood cell would be like truck drivers, our immune system the police and so on. Every cell must do its job for the body and/or society to function and it seems to require sophisticated measures to ensure that ever unit is contributing to the functionality of the entity of which it is part of.

One could also think of each tissue type as a different species and then our body would be an ecosystem, each cell type a species and each cell an individual member of its species//cell type. Anyhow, regardless how we look at it, we seem to have a reasonably although not perfectly functioning set of rewarding and penalizing measures at least good enough for our society to function the way it does. Would we still be as productive and efficient as on an overall social level if everyone could do as desired and there be no socially administered rewards and penalties? So it seems to work on a social level, but how about on the level of each species?

Who can only have children? What are the minimally and sufficient requirements for having children? Easy answer - one must at least have reached sexual maturity implying that one lived successful for at least about a decade. The youngest mother was nine years old by the way. Therefore, any severely mutated conceptual product would never even be born and those who are more challenged than others have lower chances for reproducing due to the merciless forces of negative social Darwinistic selection. But how could we positively select for those cells, who are most beneficial to our organism, i.e. rewarding them by raising the odds for their reproduction, and to prevent harmful cells, such as cancers, from replicating at all and thus to penalize them by limiting their negative overall impact to themselves until we'll discover better mechanisms allowing us to selectively kill them (negative selection)?

Let’s derive our solution from evolution of methods of reproduction of higher organisms, who exclusively reproduce sexually, with more primitive species, who can reproduces sexually and asexually? Did you ever wonder why in most species individual members must overcome some hurdles before they can reproduce? Would it be advantageous to require 3 or even more people to have children? Is an increased complexity of the reproductive pathways beneficial or harmful? What advantages have sexually reproducing species over those that primarily reproduce asexually by simply forming clones of themselves? Why is asexual reproduction still around?

Now the main question, I have never been able to address before is how to generate transgenic exclusively sexually reproducing cells, how to prove that they are less susceptible to develop cancer and to live linger than their asexually reproducing counterparts? Now before starting to address this question, lets conduct a thought experiment proving that a population consisting of members exclusively composed of sexually reproducing individual cells are less prone to cancer, live longer and adapt faster to changes in their environment than their asexually reproducing respective counterparts.

Lets do the cancer first by attempting to answer the question how sexually reproducing cells should ideally differ from their asexual precursors.

Lets imagine 2 multicolor specs whose members are organism consisting of a single identical cell type which are only differ in their way of reproduction. But how in the world, would a transgenic cell need to be designed in order to exclusively reproduce sexually?

First of, it must be haploid unless we want to become tetraploid (having 4 of each chromosome instead of 2 [diploid] chromosomes. We need something similar to miosis rather than mitosis. And we'd need to code for sex-specific differences among both sexes of each particular cell types. Can you imagine cells being pretty, hot and sexually attractive? How can we combine cellular sexual attractiveness with subsequent increased contributions of their progeny cells to the whole body?

Let’s worry about the design first:

In nature, we have X and Y chromosomes. In order to have sex-specific differences among the cells of the same type, we could just express both sex chromosomes. We could however, change the proteins the sex genes are coding for because there is no way to transform all sexually induced differences between men and women down to the level of a single cell. But it would conceivably be possible to express male and female specific proteins on their cell surface. Then they'd need a way to recombinant and combine their DNA and to exchange homologous portions of their chromosomes in order to try new variations causing homologous recombination thus - by trial and error - selecting for those progeny cells that are contributing even more to the body as a whole than the progenitor cells from which they are derived. If we could somehow achieve this, we'd quickly adapting much better to environmental changes without even having to do anything, e.g. drugs, gene therapy, human-machine hybrid, nanobots to ensure our survival. Inducing such a self-regulating adaptive mechanism is imperative because we are changing our environment so rapidly that otherwise - we'd had no chance to adapt to it in a timely manner. And this would allow us to adapt subconsciously because our body will only be composed of those cells that are most beneficial for its survival, physiological and social success!!! This could be termed individualized self-perpetuating evolution which could even result in speciation events due to our different work and living environments, to which everybody could adapt much more rapidly, would widen the genetic gaps between different professions until they can no longer have viable progeny and therefore defining them as different species. Cool! I never thought of that.

But now back to our wish list and expectations to be met when designing exclusively sexually reproducing cells. Apart from the required sex-specific differences, we'd need a genetically encoded sex-specific set of mating procedures. Should we design them rather simple or complex?

I'd lean towards complexity because random mutations induced by mutagens and carcinogens, such as radiation, free radicals, intercalating chemicals and nuclear viral gene and viral gene integration are more likely to cause loss-of-function mutations in the genes that must be expressed to reproduce sexually, if there are more of them and which are hence comprising a larger percentage of the overall genome. Therefore, if a random mutagen is inducing cancer-causing mutations, it is also more likely to cause loss of function mutations in those genes required for sexual reproduction.

Have you ever looked at the karyottype (visualization of its condensed chromosomes) of a cancer cell and compared it to their healthy controls? If not, compare the two pictures below:

Below you see a healthy human karyotype. All of its chromosomes are stained and then nicely arranged into their respective pairs

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Now compare the healthy karyotype above with that of a long cancer cell shown below:

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Can you see how abnormal it is? Instead of chromosome pairs, we see three instead of two, in some cases and others, like the Y or the second X chromosome (depending on whether the cancer victim was a male or a female) is completely missing. Any abnormal number of chromosomes that are not paired (2 of each) except for X and Y is referred to as unemploiedy

Can you imagine a cell with the karyotype below to be able to replicate? It shouldn't right? But unfortunately it does because otherwise its poor carrier would not be suffering from the final stages of lung cancer. Wouldn't it be cool to prevent a similar abnormal and cancer causing karyotype from replicating? Even if such a cancer cell could still manage to have sex, more than likely, its progeny would not be viable thus interrupting the vicious cycle of metastasizing. In cancer cell similarly nasty kearyotype as shown above are still replicating and due to the problems caused by the anemploiedy, are mutating even faster thus setting the evolutionary stage of trial and error for the cancer to become even more aggressive and drug tolerant because by giving anti-cancer drugs, we are inevitably selecting for those cancer cells that are possessing mutations which are rendering them more insensitive to a previously effective anti-cancer drug. Setting the barrier for replication higher than it is currently for asexual cellular reproducing would exclude many cancer cells with abnormal karyotype (anemploiedy) for replicating. However, to ensure the beneficial - especially cancer cell replicating inhibiting effects inherent to using only sexually reproducing cells; we'd need to knock out all genes required for asexual reproduction but not for sexual reproduction. Since I am expecting the metabolic and signal transduction pathways required for sexual and asexual reproduction to overlap significantly, we probably cannot get rid of all genes involved in the traditional asexual cellular reproduction of somatic cells. Nevertheless, knocking out only a few genes, which are exclusively required for asexual reproduction (i.e. simple traditional cell division) would lower the probability for carcinogenic gain-of-function mutations, which should remain silenced because they have been deleted in the first place.

Now how could sexually reproducing cells find their respective mating partner and how can we ensure that different cell types don't mate, since they have no eyes and don't even have any glue to which cell type they belong?

Similar to viruses, which are binding very specifically to very unique surface proteins of their host cells, in order to infect them, male and female cell surface recognition and binding should be highly specific and even unique for each cell type. A very crude example of intercellular sex can be observed when E-coli transfer plasmids that are coding for proteins, which are rendering the plasmid-receiving E-coli bacterium less sensitive to a particular antibiotic to which it is exposed. Can you now appreciate the advantage of sexual over asexual reproduction? Giving cells the opportunity to try out different genes to better function in a rapidly changing external environment is helping a lot. Without it, E-coli and many other bacterial species, which have now become resistant to our antibiotics, might otherwise already be extinct a few years ago. But instead, despite our efforts to kill them, they keep striving better than ever, often pushing our methods of medical intervention very close to and sometimes even beyond their limits, e.g. according to recent very alarming reports from Sweden, the previously deemed harmless tripper bacterium causing Gonorroe is on its way of becoming resistant against every antibiotic that we have. And plasmid transfer via pilli is not even close to the mechanism, which I envision to regulate the reproduction of the mentioned transgenic cells on many levels, thus giving us many targets to intervene in case we ever encounter carcinogenesis among those cells. This probability is not zero because similar to trisomy 21, as it is the case for humans living with 3 instead of 2 chromosomes 21, the replication of anemploitic cells can never be completely ruled out.

Let’s summarize our wish list for our new transgenic sexually reproducing somatic cells before getting into more details how we could go about generating them.

Our transgenic exclusively sexually reproducing cells must:

1. Express sex-specific genes

2. Replicate by meiosis rather than mitosis

3. Mast have cell surface binding proteins, which are not only sex-specific but also unique to each cell type

4. Knock outs of all genes, which are exclusively required for asexual reproduction but for nothing else.

But how can we ensure that those cells, who contribute most to the organism, have higher chances of replicating? How can we reward them? How can we quantify their overall benefit to cost ratio and compare it to other cells? Howe can we ensure that the next cell generation is superior to the previous one?

We may actually be much closer to this utopically seeming goal because the major obstacle is that - despite trying at least since 1980, we are still lacking the skill of site directed expression vector integration. We are now capable of site-directed mutagenesis, i.e. we can alter any DNA sequence down to a single nucleotide using Kunkel's methods for plasmids and Mega Primer for linear DNA. However, unfortunately we are still lacking the skill of specifying the location in the genome at which we'd like our expression vector to integrate into the host genome. As soon as we have mastered this crucial skill, we are probably not very far from generating the transgenic cells envisioned above because it would allow us to take any gene from any organism and insert it into our genome. Moreover, we could even express any inserted expression vector at will by simply designing its promoter such that an inducer similar to IPDG is required to modify its transcription level. Even much more sophisticated integrated expression vector regulation models similar to those I have described in the second half of my second molecular biology exam in early May 2012 are then within reach. I just must find the time to search for the word file of this exam in order to specify the technique. So far, I can only remember that SV-40 RNA polymerase was expressed epigenetically on a plasmid or in the nuclear genome and that it required IPGD to turn it on. Then this very powerful viral RNA polymerase was transcribing the gene of interest coded for on another plasmid thus providing multiple levels to regulate gene expression and to even counteract the problem that of very low basal transcription of the viral RNA polymerase gene even when a repressor - which could also be given to the cells to turn off certain genes - is supposedly - at least in theory - preventing its transcription. I cannot comprehend however, how - if there is absolutely no space for RNA polymerase to bind to its target sequence because a repressor has already bound to it very tightly - can still manage to minimally transcribe such a gene unless not every absolutely necessary RNA polymerase binding regions is covered by a repressor all the time (leaky repressor binding).

Dr. Yuri Vozianov's experiments with Cre-Lox recombination, which Manju, my tutor at Louisiana Tech explained to me, might be a promising approach towards achieving site directed expression vector integration because it is working just fine during mitosis where homologous DNA segments are cleaved out, exchanged in ligated into the other strand. Since genes are often subject to homologous recombination during meiosis, this DNA segment exchange mechanism, must function down to the precision of a single nucleotide because otherwise, we'd encounter many frame shift mutations. But how does it work? How do the Cre-Lox recombinases, which I believe to be a mixture consisting of restriction enzymes and ligase, "know" where to cut out and where to insert the homologous DNA segments? Maybe it’s not even a restriction enzyme because due to allelic variation a particular restriction site on one chromosome may not even be on the other, hence cutting and ligating would be impossible. But since it works there must be a way to control it. We only must find it!!!!! It is there!!! That is probably why Dr. Vazionov was only one of the 2 biology professors at Louisiana Tech University (a very small school), who had an RO1 grant for his lox recombinase research.

The features that we could add to our genome as soon as we mastered site directed expression vector integration are almost endless since there are so many species, which can do almost everything we can - but only better, except maybe for thinking and trying very hard to manipulate evolution.

We could combine the sonar and immune system of a bat, who doesn't get sick despite having high concentrations of pathogens in its blood, with the smell and hearing of a dog, the vision acuity of an eagle and the photoreceptor diversity of a turtle, which is a penta-chromate. Having 5 instead of 3 different color photo receptors, would help me out a lot in remembering because due to my synthestsia, I can much better remember anything with which I can associate a color.

Since - in my brain - every letter and every number has its uniquely specific color, the color of a word or number is the average of the colors obtained when combining their single character components. Therefore, it is helping me a lot to write terms, which are difficult for me to remember, with the colors of their respective letters in order to remember them better in the exam. Hence, if I don't know how to spell a long complex word, I cannot remember it easily and since I am also dyslexic making it even harder for me to retain spellings, I am often trapped in a vicious cycle of not being able to remember because I cannot spell while finding it very challenging to spell due to my dyslexia, which again is then preventing me from retaining new terms hence requiring me to spend almost my entire life studying for exams and completing assignments even past their deadline because I'd simply had no chance to meet it no matter hat I am trying. But being able to distinguish between more colors - like a turtle can (it can even see UV light), would help me a lot in memorizing. I am always having the strange feeling that there are simply not enough colors in this world and way too many objects thus leaving me no other option than having to assign the same color to multiple objects, ideas, words and/or concepts. This in turn is contributing to confusion because if the colors that I am associating with 2 different words are too close, I'll get them mixed up. For examples, somehow the words "representation" and "precipitation" are invoking almost the same color sensation in my brain making it hard for me to keep them apart. This is not surprising however, because their length and letters are very similar, especially since I am subconsciously associating almost the same color with the letters "e", "p" and "c, which are the most common characters in both words. But if we could express the genes for any photoreceptor from any species, I would have almost endlessly many different colors that I could then associate with any entity I am encountering and it would be advantageous to relate more reliably to many more objects by assigning a color to them.

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27 Views

What happens during male pubertal growth?

Question

Nov 2011

Male-female sexual differentiation is completed by the late second trimester of prenatal gestation (Gluckman, et al., 1980; Grumbach & Styne, 1992). Between the 11th and 24th weeks of fetal life, a higher concentration of circulatory testosterone occurs in males in response to (1) placental gonadotropins (Greek: gone = seed; trope = nourishment for growth) and (2) release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland into the circulatory system. The testosterone is released from the fetal testes and it interacts with bodywide physicochemical processes to further develop uniquely male characteristics. In females, gonadotropins, LH, and FSH trigger the circulatory release of estradiol from the fetal ovaries, and estradiol interacts with bodywide physicochemical processes to further develop uniquely female characteristics.

The greater concentration of testosterone in males continues until just before birth when it is temporarily suppressed. Within just a few minutes following the birth of males, however, the concentration of peripheral circulatory luteinizing hormone (LH) increases by about ten times the level that was present before and during birth. LH levels then recede, but the spurt triggers the release of circulatory testosterone that lasts about 12 hours or more. LH levels then become more moderate, but greater LH pulsatility and more elevated testosterone levels continue for about six months, after which their levels are biochemically suppressed (not eliminated) until puberty (Grumbach & Kaplan, 1990; Grumbach & Styne, 1992).

The greater concentration of estradiol in females continues until just before birth when it is temporarily suppressed. No post-birth surge of LH release occurs in females. There is, however, a rise in levels of circulatory FSH and LH and it is irregularly pulsatile during the first few post-birth months. FSH pulsatility is then greater in females than in males for the first few years of life, resulting in greater levels of circulating estrogens. In general, greater FSH pulsatility and estrogen levels continue for about one to two years, after which their levels are biochemically suppressed (not eliminated) until puberty (Grumbach & Kaplan, 1990; Grumbach & Styne, 1992).

All of the anatomic components that produce voice are formed during prenatal gestation, and most begin functioning in some way before birth. The macro-architecture of voice-related anatomy is significantly smaller at birth compared to adult dimension; proportional relationships are significantly different; and anatomic micro-architecture is in very early stages of maturation. Middle and inner ear structures, however, are comparable to adults by about five months gestation (see later details). Physical growth of vocal anatomy progresses throughout childhood, but is notably extensive during the first 3 to 5 years and during puberty.

Puberty (Latin: pubertas = age of maturity) is one macro-growth phase in the continuum of human physical development. On average, it begins in females at about age 10 years and extends to about 16 years. In boys, it begins at about age 12 years and extends to about 18 years (Grumbach & Styne, 1992). During puberty there is observable growth in (1) standing and sitting height, (2) gross body weight, (3) lean body tissue (muscles and organs) and fat body tissue, (4) body hair, and (5) various anatomic and organ areas of the body such as feet, hands, gonads, pulmonary system, larynx, vocal folds, vocal tract, and various areas of the central nervous system (notably in the prefrontal cortex).

The initiation of puberty is triggered by: (1) cessation of biochemical suppression of the hormones of growth, and (2) elevated synthesis and release—from the hypothalamus into the anterior pituitary—of gonadotropin-releasing hormone (GnRH) [formerly known as luteinizing hormone-releasing hormone (LHRH)]. GnRH triggers the synthesis of luteinizing hormone (LH) and follicle stimulating hormone (FSH) and they are then released from the anterior pituitary into the circulatory system. An increase in both the frequency and amount of these hormones occurs. Elevated LH and FSH stimulate the release into the bloodstream of the anabolic (growth) steroids: (1) primarily testosterone in males with some estradiol, and (2) primarily estradiol in females with some progesterone. These events, plus many others, result in the anatomical growth spurts in height, weight, tissue and organ size, cognitive-emotional behavior changes (Warren & Brooks-Gunn, 1989; Michael & Zumpke, 1990), and so forth.

The years-long time scale release of these hormones and steroids produce the years-long pubertal macro growth phase. Within the pubertal macro-growth phase, however, there are shorter time-scale growth episodes that span multiple weeks to multiple months. During those growth episodes, the triggering hormones enter the circulatory system in pulsatile spurts that last anywhere from 5 to 10 minutes to one hour or more, and they occur mostly during the earlier stages of nightly sleep (Grumbach & Styne, 1992; O'Dell, 1995).

The growth episodes occur in sequential stages within the various anatomical areas of the body, but the time of initiation and the duration of each stage is different in each individual (Nielsen, et al., 1986; Wennick, et al., 1988; Martha, et al., 1989; Dunkel, et al., 1990; Hassing, et al., 1990; Grumbach & Styne, 1992; Lampl, et al., 1993; Vander, et al., 1994, pp. 627-629; O'Dell, 1995). For instance, the end-areas of both limbs (hands and feet) grow larger first, and then the bones and soft tissues of the arms and legs grow longer and larger. Increases in glove and shoe sizes, therefore, "announce" increases in general clothes sizes. Tanner (1972, 1984) devised five-stage evaluative scales of breast development in females and genital development in males to assist pediatricians in assessing normal versus abnormal pubertal development. Tanner's episodic stages of genital development in male adolescents have been correlated with their voice transformation stages (Harries, et al., 1996).

An adolescent does not go to bed one night and wake up the next morning with mature breasts and genitals, nor do their feet need shoes that are one or two sizes larger than the shoes they wore the previous day. These growth processes do not literally happen "overnight". Over many nights, specified recipes of growth hormones interact with their biochemical receptor sites on the cells of specified target tissues and organs. Intracellular physicochemical processes are then triggered in the cells of those tissues and organs so that some cells within just hands, or feet, or legs, or arms, or larynges start dividing into more cells faster than they did before. So, elevated growth hormone, testosterone, and estradiol levels are followed by physical growth processes which activate for a period of time, then subside, then activate, then subside, and so on in an evolving, longer-term, episodic pattern (Grumbach & Styne, 1992; O'Dell, 1995). The "choreography" of these complex pubertal growth processes is unique in each person.

The continuum of human growth in prenatal, childhood, and pubertal age spans are reflected in the growth patterns of the respiratory system, the larynx, and the vocal tract. The end-age parameter of the "young" voice is established by the Hirano, et al., finding (1981) that nearly all of the macro- and micro-architecture characteristics of adult laryngeal anatomy have been completed by about age 20-21. One important evolution of micro-architecture is not substantial until ages 28 through 32, that is, calcification and ossification of the hyaline laryngeal cartilages. This change usually proceeds earlier in males than females (Hately, et al., 1965; Kahane 1983).

REFERENCES

Dunkel, L., Alfthan, H., Stenman, U., et al. (1990). Pulsatile secretion of LH and FSH in prepubertal and early pubertal boys revealed by ultrasensitive time-resolved immunofluorometric assays. Pediatric Research, 27, 215-219.

Gluckman, P.D., Grumbach, M.M., & Kaplan, S.L. (1980). The human fetal hypothalamus and pituitary gland: The maturation of neuroendocrine mechanisms controlling the secretion of fetal pituitary growth hormone, prolactin, gonadotropin, and adrenocorticotropin-related peptides. In D. Tulchinsky, & K. Ryan (Eds.), Maternal-Fetal Endocrinology (pp. 196-232). Philadelphia: W.B. Saunders.

Grumbach, M.M., & Kaplan, S.L. (1990). The neuroendocrinology of human puberty: An ontogenetic perspective. In M.M. Grumbach, P.C. Sizonenko, & M.L. Aubert, (Eds.), Control of the Onset of Puberty (pp. 1-68). Baltimore: Williams & Wilkins.

Grumbach, M.M., & Styne, D.M. (1992). Puberty: Ontogeny, neuroendocrinology, physiology, and disorders. In Wilson, J.D., & Foster, D.W. (Eds.), Williams Textbook of Endocrinology (8th Ed., pp. 1139-1221). Philadelphia: W.B.Saunders.

Harries, M.L.L., Griffin, M., Walker, J., & Hawkins, S. (1996). Changes in the male voice during puberty: Speaking and singing voice parameters. Logopedics Phoniatrics Vocology, 21(2), 95-100.

Hassing, J.M., Padmanabhan, V., Kelch, R.P., et al. (1990). Differential regulation of serum immunoreactive luteinizing hormone and bioactive follicle-stimulating hormone by testosterone in early pubertal boys. Journal of Clinical Endocrinology and Metabolism, 70, 1082-1089.

Hateby, B.W., Evison, G., & Samuel, E. (1965). The pattern of ossification in the laryngeal cartilages: A radiological study. British Journal of Radiology, 38, 585-591.

Hirano, M., Kurita, S., & Nasashima, T. (1981). The structure of the vocal folds. In M. Hirano (Ed), Vocal Fold Physiology. Tokyo: University of Tokyo Press.

Kahane, J.C. (1983). Postnatal development and aging of the human larynx. Seminar in Speech and Language, 4, 189-203.

Lampl, M., Veldhuis, J.D., & Johnson, M.L. (1993). Saltation and stasis: A model of human growth. Science, 258, 801-803.

Martha, P.M., Rogol, A.D., & Veldhuis, J.D. (1989). Alterations in the pulsatile properties of circulating growth hormone concentrations during puberty in boys. Journal of Clinical Endocrinology and Metabolism, 69, 563-570.

Michael, R.P., & Zumpke, D. (1990). Behavioral changes associated with puberty in higher primates and the human. In M.M. Grumbach, P.C. Sizonenko, & M.L. Aubert (Eds.), Control of the Onset of Puberty. Baltimore: Williams & Wilkins.

Nielsen, C.T., Skakkebaek, N.E., Darling, J.A., et al. (1986). Longitudinal study of testosterone and luteinizing hormone (LH) in relation to spermarche, pubic hair, height and sitting height in normal boys. Acta Endocrinologica [Suppl], 279, 98-106.

O'Dell, W.D. (1995). Endocrinology of sexual maturation. In DeGroot, L., et al., Endocrinology (3rd Ed., Vol. 2, pp. 1938-1952). Philadelphia: W.B. Saunders.

Vander, A.J., Sherman, J.H., & Luciano, D.S. (1994). Human Physiology: The Mechanisms of Body Functions (6th Ed.). New York: McGraw-Hill.

Warren, M.P., & Brooks-Gunn, J. (1989). Mood and behavior at adolescence: Evidence for hormonal factors. Journal of Clinical Endocrinology and Metabolism, 69, 77-83.

Wennick, J.M., Delemarre-Van de Waal, H.A., van Kessel, H., et al. (1988). Luteinizing hormone secretion patterns in boys at the onset of puberty, measured using a highly sensitive immunoradiometric assay. Journal of Clinical Endocrinology and Metabolism, 67, 924-928.

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