Unit 5: Respiration, Internal Environment, Coordination and Gene Technology

Aerobic respiration transfers energy from glucose to ATP using oxygen, producing carbon dioxide and water. Glycolysis occurs in the cytoplasm; the link reaction and Krebs cycle occur in the mitochondrial matrix; oxidative phosphorylation occurs on the inner membrane.

Enzymes release energy in controlled steps rather than one burst. NAD and FAD carry hydrogen/electrons between stages, while ATP provides immediately usable energy for cellular work.

A defect in the inner membrane can disrupt electron transport and ATP synthase even if glycolysis in the cytoplasm continues for a time.

The word “energy” is not a product that floats free: it is transferred into ATP and heat. Keep substrate, ATP yield, location and oxygen requirement distinct.

Glycolysis takes place in the cytoplasm and does not require oxygen. Glucose is phosphorylated and split into triose phosphate; oxidation then produces two pyruvate, four ATP gross (two net) and two reduced NAD.

The initial ATP investment makes glucose more reactive. Reduced NAD carries hydrogen to later stages when oxygen is available, while pyruvate can enter fermentation when it is not.

Two ATP are used at the start and four are formed later, so the net gain is two ATP per glucose, not four.

Glycolysis is not the complete aerobic pathway and does not require mitochondria. A reduced-NAD molecule is not the same thing as ATP.

In the mitochondrial matrix, pyruvate is decarboxylated and dehydrogenated, forming acetyl CoA, carbon dioxide and reduced NAD. Acetyl CoA then joins oxaloacetate; the Krebs cycle releases CO₂, reduces NAD/FAD and makes ATP while regenerating oxaloacetate.

Each glucose produces two pyruvate, so the link reaction and cycle turn twice per glucose. The cycle is sustained because the acceptor molecule is regenerated.

One glucose gives two acetyl CoA, two CO₂ and two reduced NAD in the link reaction; two turns of the cycle then yield four CO₂, six reduced NAD, two reduced FAD and two ATP.

No ATP is made directly in the link reaction. The Krebs cycle is not “in the mitochondrion” generally; its matrix location and carbon accounting matter.

Reduced NAD and FAD donate electrons to the inner-membrane electron transport chain. Energy released pumps protons into the intermembrane space; their return through ATP synthase drives ADP phosphorylation.

Oxygen is the final electron acceptor, combining with electrons and protons to form water. Without oxygen, carriers remain reduced, proton pumping stops and oxidative ATP production collapses.

A proton gradient is like stored potential energy: blocking ATP synthase prevents its controlled use, while making the inner membrane leaky dissipates the gradient as heat.

Chemiosmosis is not direct phosphorylation by oxygen, and the exact ATP yield depends on the accounting convention. Keep proton gradient, ATP synthase and final acceptor separate.

When oxygen is limited, the electron transport chain and Krebs cycle cannot continue normally. Reduced NAD transfers hydrogen to pyruvate, forming lactate and regenerating NAD for glycolysis.

Anaerobic metabolism yields only the small net ATP gain from glycolysis, but it can maintain short-term ATP production. Lactate can later be oxidised to pyruvate or converted to glucose when oxygen is available.

After intense exercise, deeper breathing supplies extra oxygen for processing lactate; the increased ventilation is not evidence that anaerobic respiration itself produced more ATP.

Lactate formation does not make oxygen irrelevant and does not create a large ATP yield. Separate immediate fermentation from later oxygen debt recovery.

Respiratory quotient (RQ) is calculated as CO₂ produced divided by O₂ consumed during respiration. The value helps infer which respiratory substrate is being used, provided the measurements refer to the same time period.

Use gas volumes or moles under consistent conditions, then compare the result with the expected quotient for the substrate. Mixed substrates or anaerobic metabolism can make interpretation less direct.

For glucose under aerobic respiration, equal stoichiometric amounts of CO₂ and O₂ give RQ = 1. A lower value can indicate a lipid-rich substrate because proportionally more oxygen is required.

RQ is not a direct measurement of ATP yield, and a quotient from mixed or anaerobic respiration cannot be assigned to one pure substrate without qualification.

A respirometer measures oxygen uptake by a respiring organism. Soda lime or potassium hydroxide absorbs produced carbon dioxide, so the fall in gas volume reflects oxygen consumption.

Use a control with glass beads, keep temperature constant, measure capillary movement over time, reset between repeats and convert the movement using the capillary radius and distance.

If the manometer moves 2 cm in one minute and the capillary radius is r, the volume change is πr²h per minute; averaging repeats gives a more reliable rate.

Movement is not automatically oxygen volume unless CO₂ is absorbed and pressure/temperature are controlled. Living organisms require humane handling.

A respirometer can estimate oxygen consumption; respiratory quotient compares CO₂ produced with O₂ consumed. Both are rates or ratios that require the same time interval and controlled conditions.

Use a control, repeat measurements, absorb CO₂ only when the design requires oxygen uptake, and keep organism mass, temperature and activity comparable. Calculate RQ from gas volumes or moles.

A rise in oxygen uptake after warming may reflect faster respiration, but if temperature also changes gas pressure the apparent rate is confounded unless the control corrects it.

RQ from mixed substrates or anaerobic metabolism is not a clean substrate fingerprint. Separate instrument movement, oxygen consumption and the final quotient.

Muscles generate pulling force; bones resist bending and act as levers. Tendons connect muscle to bone and transmit force, while ligaments connect bone to bone and stabilise joints.

Because a muscle cannot push, opposing muscles work antagonistically around a joint. One contracts while its partner relaxes to reverse the movement.

To flex the elbow, biceps contract and triceps relax; to extend it, triceps contract and biceps relax. The bone provides the rigid structure being pulled.

Tendons are not ligaments, and a relaxed antagonist is not necessarily inactive in every movement. Identify the joint action and force direction.

Fast-twitch fibres contract rapidly and suit short, high-intensity activity; slow-twitch fibres contract more slowly and resist fatigue during sustained activity. Their structure and metabolism support those roles.

Fast fibres rely more on anaerobic ATP supply and have fewer capillaries and less myoglobin; slow fibres have greater aerobic capacity, blood supply and oxygen storage.

A sprint uses fast fibres for rapid force, whereas prolonged walking recruits more slow fibres. A muscle usually contains a mixture rather than only one fibre type.

“Fast” does not mean stronger in every task, and fibre type alone does not determine performance. Link the claim to ATP pathway, fatigue and activity duration.

An action potential releases calcium from the sarcoplasmic reticulum. Calcium binds troponin, moves tropomyosin away from actin sites, and allows myosin heads to form cross-bridges and pull actin towards the sarcomere centre.

ATP lets a myosin head detach and its hydrolysis resets the head for another power stroke. Repeated cycles bring Z discs closer; when calcium is pumped back, binding sites are blocked and relaxation follows.

The filaments remain the same length while the sarcomere shortens. Without ATP, myosin cannot detach, explaining rigor mortis after death.

ATP is needed for detachment as well as the recovery stroke, and calcium exposes binding sites rather than directly pulling actin.

The sinoatrial node initiates a myogenic wave; the atria depolarise and contract, the atrioventricular node delays transmission, and Purkyne tissue spreads excitation through the ventricles from the apex.

On an ECG, the P wave reflects atrial depolarisation, the QRS complex ventricular depolarisation and the T wave ventricular repolarisation. Wave timing and rhythm reveal coordination, not blood pressure directly.

A prolonged interval or irregular rhythm can suggest conduction or fibrillation problems, while a low resting rate in a trained athlete may be normal bradycardia.

An ECG is an electrical trace, not a direct image of contraction force or a diagnosis by itself. Interpret the wave, interval and clinical context together.

Cardiac output is the volume pumped by a ventricle per minute: cardiac output = heart rate × stroke volume. It rises during exercise so working cells receive more oxygen and substrates.

Keep units consistent, convert cycle time into beats per minute, then rearrange the equation when heart rate or stroke volume is unknown.

If one cardiac cycle lasts 1.2 s, heart rate is 60 ÷ 1.2 = 50 bpm. With stroke volume 75 cm³, cardiac output is 3,750 cm³ min⁻¹ or 3.75 dm³ min⁻¹.

A higher heart rate does not always mean a higher cardiac output if stroke volume falls. Cardiac output is a volume per time, not the blood pressure itself.

Adrenaline is released during acute stress and prepares the body for rapid action. It increases heart rate and ventilation, redirects blood toward skeletal muscle and raises blood glucose availability.

The response is coordinated by receptors and effectors: more cardiac output and ventilation deliver oxygen, while glycogen breakdown supplies respiratory substrate. It is rapid and short-term rather than a complete long-term adaptation.

A sudden threat can cause heart rate to rise before movement begins, increasing cardiac output; the same response can be unnecessary or costly if stress is prolonged.

Adrenaline does not directly create ATP and “fight-or-flight” is not a single switch. Identify the target tissue and physiological effect.

During exercise, ventilation increases to bring in more oxygen and remove more carbon dioxide. A spirometer can record breathing volume over time so rate, tidal volume and total ventilation can be compared.

Calibrate the apparatus, keep posture and workload consistent, collect repeated traces and distinguish breathing rate from depth. Use a control or resting trace for comparison.

A person may increase ventilation by breathing deeper, faster or both. A larger trace area does not automatically mean a higher oxygen uptake unless the gas measurement is calibrated.

Spirometry measures air movement, not directly ATP production. Leaks, mouthpiece position and exercise intensity can distort the trace.

A homeostatic control system detects deviation from a set point and coordinates effectors. Negative feedback opposes the deviation and returns the variable toward its normal range; positive feedback reinforces a change until a defined endpoint.

Thermoregulation increases heat loss when body temperature rises, whereas clotting can amplify activation until a wound is sealed.

Homeostasis is dynamic equilibrium, not a perfectly fixed value. Do not label every response negative or assume positive feedback is automatically unstable.

When body temperature rises, vasodilation and sweating increase heat loss; when it falls, vasoconstriction, shivering and raised metabolic rate reduce heat loss or generate heat. Receptors and effectors maintain a narrow operating range for enzymes.

Vasoconstriction reduces heat loss rather than directly warming the blood. Sweating works by evaporation, so humidity changes its effectiveness.

In humid air, sweat may remain on the skin while evaporation slows; in cold air, vasoconstriction diverts blood from surface capillaries and shivering raises respiration.

Thermoregulation is not a single “set temperature” response and skin redness does not itself mean core temperature is safe.

The mammalian kidney maintains water and solute balance by filtration at the glomerulus, selective reabsorption along the nephron and controlled water permeability in the collecting duct.

Small molecules enter the filtrate under pressure, but cells and large proteins remain in the blood. Useful glucose, ions and water are reabsorbed according to body needs; hormones such as ADH alter collecting-duct permeability.

When blood water potential falls, more ADH increases aquaporins in collecting-duct membranes, so more water returns to the blood and urine becomes concentrated.

Filtration is not the same as excretion, and urine concentration is not controlled by “the kidney” as one undifferentiated organ. Separate nephron region, substance and hormone.

Amino-acid deamination produces ammonia, which is toxic. In the liver, the urea cycle converts ammonia into urea, a less toxic soluble compound transported in the blood to the kidneys.

Urea can be filtered and excreted in urine, allowing nitrogen from excess amino acids to leave the body without ammonia accumulating in tissues.

After a high-protein meal, more amino acids may be deaminated; increased urea production reflects nitrogen disposal, not direct protein storage.

Deamination is not the same as digestion, and urea is not formed in the nephron. Keep liver conversion, blood transport and kidney excretion separate.

High pressure forces water and small solutes from glomerular blood into Bowman’s capsule. Cells and large proteins remain in the blood; useful substances are then selectively reabsorbed along the nephron.

The loop of Henle establishes a medullary water-potential gradient, allowing the collecting duct to reabsorb water when hormone signals make it permeable.

Glucose is normally reabsorbed early in the nephron, while water reabsorption varies with body water status. A substance in filtrate is not automatically destined for urine.

Ultrafiltration is pressure-driven, whereas selective reabsorption is transport-based. Do not call every nephron segment equally permeable or equally responsible for concentration.

Osmoreceptors detect blood water potential and the hypothalamus/pituitary adjusts ADH release. ADH increases aquaporins in collecting-duct membranes, so more water returns to the blood and urine becomes concentrated.

When blood is dilute, less ADH leaves the collecting duct less permeable and more dilute urine is produced. The response is negative feedback around a regulated water balance.

After dehydration, high ADH increases water reabsorption even though the filtered load may be similar; the final urine changes because permeability changed.

ADH does not “add water” to urine and does not act equally on every nephron segment. Separate sensor, hormone, membrane change and final urine effect.

A transcription factor is a protein that binds a regulatory DNA sequence and changes whether RNA polymerase can transcribe a gene. Hormone receptors can act as transcription factors when a lipid-soluble hormone enters a cell and binds them.

Changing transcription changes mRNA production, which can change protein amount and therefore cell behaviour. Different cells respond differently because they express different receptors and target genes.

A steroid hormone–receptor complex can enter the nucleus, bind DNA and increase transcription of a target gene; a peptide hormone usually signals through a membrane receptor instead.

A transcription factor does not translate mRNA or guarantee a phenotype. Distinguish receptor location, DNA binding, transcription and downstream protein function.

Neurones carry electrical impulses. A cell body maintains the cell, an axon conducts the impulse and axon terminals connect with other cells; myelin insulates some axons so impulses jump between nodes of Ranvier.

Sensory neurones carry information from receptors to the CNS, relay neurones connect within the CNS, and motor neurones carry signals to muscles or glands. Their structures reflect these routes.

A myelinated axon can transmit faster because depolarisation occurs at nodes rather than along every section of membrane.

A nerve is a bundle of neurones, not one giant neurone. Do not infer function from myelination alone without identifying the pathway.

The basic pathway is stimulus → receptor → sensory neurone → CNS → motor neurone → effector. The CNS integrates information and the effector produces a response through muscle contraction or gland secretion.

Bright light activates retinal receptors; impulses reach the CNS and motor neurones stimulate circular iris muscles so the pupil constricts. In low light, radial muscles contract and the pupil dilates.

Antagonistic effectors allow opposite outcomes, while a rapid neural pathway limits exposure to harmful conditions.

A receptor detects a change but does not itself perform the response. Keep sensory input, CNS coordination and effector action distinct.

A reflex arc routes a stimulus from receptor through a sensory neurone and relay neurone in the CNS to a motor neurone and effector. The response is rapid and protective, reducing delay from conscious decision-making.

Synapses determine direction and integration, while antagonistic muscles can create the final movement. The brain can receive information about the stimulus even though the immediate arc is local.

Touching a hot surface activates pain receptors; flexor muscles contract and opposing extensors relax before the person consciously interprets the pain.

A reflex is not an absence of the brain and not every rapid movement is a simple spinal reflex. State receptor, CNS relay, effector and response.

When membrane depolarisation reaches threshold, voltage-gated sodium channels open and sodium ions enter. Potassium ions then leave to repolarise the membrane; the signal propagates as neighbouring sections reach threshold.

The all-or-nothing action potential is regenerated along the axon, so its amplitude does not fade with distance. Refractory periods help maintain one-way transmission.

A stronger stimulus is represented by more frequent action potentials, not a larger action potential, once threshold has been crossed.

Threshold is not a graded “bigger signal”, and ion movement is not the same as the whole impulse physically travelling as one sodium wave.

In a myelinated axon, the sheath insulates the membrane between nodes of Ranvier. Depolarisation is regenerated at the nodes, so the impulse appears to jump along the axon by saltatory conduction.

The insulation reduces ion leakage and increases conduction speed compared with a non-myelinated axon, where the membrane is activated continuously.

Damage to myelin can slow or disrupt signalling even when the axon and its cell body remain present, because the normal node-to-node pattern is lost.

Saltatory conduction does not mean the impulse skips the cytoplasm entirely, and a nerve is a bundle of axons rather than one myelinated cell.

An action potential opens calcium channels in the presynaptic knob. Calcium triggers vesicles to release neurotransmitter, which diffuses across the cleft and binds receptors on the postsynaptic membrane, opening ion channels.

Transmission is one-way because release and receptors are on opposite sides. Summation of repeated or converging inputs can bring the postsynaptic membrane to threshold.

At the pupil pathway, receptor impulses reach the CNS and motor neurones activate antagonistic iris muscles; synapses ensure the signal is routed rather than reflected backward.

Neurotransmitter does not electrically jump the cleft, and binding is not enough unless the postsynaptic effect reaches threshold.

A drug can increase or decrease synaptic transmission by changing neurotransmitter production, release, receptor binding, breakdown or reuptake. Its effect depends on the specific step and target.

Blocking serotonin reuptake leaves more transmitter in the cleft, whereas a receptor antagonist prevents the normal transmitter from activating the postsynaptic cell.

The same principle can produce therapeutic or harmful effects: L-dopa is converted to dopamine for Parkinson’s symptoms, while recreational drugs can disrupt mood and neural control.

A drug’s effect is not simply “more neurotransmitter = better”. Identify the receptor, transmitter and direction of change before predicting behaviour.

Rod cells are photoreceptors specialised for low-light detection. Absorbed light changes the photopigment and alters ion-channel activity, which changes neurotransmitter release onto the next neurone.

Rods are sensitive but do not provide colour discrimination; their convergence improves sensitivity while reducing spatial resolution. The retina therefore transforms light into a pattern of neural signals.

In dim light, rods can detect movement at the edge of vision, whereas bright-light colour and fine detail depend more on cone pathways.

A rod cell does not send light itself and “more rods” does not guarantee sharper vision. Keep photoreceptor transduction separate from CNS interpretation.

Habituation occurs when repeated harmless stimulation produces a smaller response. The animal saves energy because fewer calcium ions enter the presynaptic neurone, less neurotransmitter is released and the postsynaptic cell is less likely to reach threshold.

A snail may take less time to re-emerge after repeated gentle touches. If the sound or touch becomes stronger, the response can return because the stimulus is no longer identical.

The change is in synaptic transmission, not a loss of all sensory ability. The animal can still respond when the stimulus becomes relevant.

Habituation is not fatigue, permanent damage or forgetting every similar stimulus. Control stimulus intensity and use a consistent endpoint when measuring it.

The central nervous system (CNS) is the brain and spinal cord; the peripheral nervous system (PNS) carries information between the CNS and receptors or effectors. Sensory and motor pathways connect the two.

This division separates integration from transmission. A receptor detects a stimulus, the CNS coordinates a response, and motor neurones carry the output to muscles or glands.

A skin receptor sends an impulse through a sensory neurone in the PNS to the spinal cord; a motor pathway then activates an effector.

The PNS is not only voluntary movement, and the CNS is not simply a cable. Identify the direction and function of each pathway.

Phytochrome exists as inactive Pr and active Pfr. Red light converts Pr to Pfr; far-red light converts Pfr back to Pr. The balance changes with day and night length and can switch flowering genes on or off.

In a long-day plant, short nights leave more Pfr, which activates gene expression leading to flowering. A far-red pulse can reverse the conversion and alter the response.

The pigment is a reversible sensor: the plant responds to the light history and duration of darkness, not simply to daytime brightness.

“Long-day” describes short-night flowering, and Pr/Pfr are pigment states rather than hormones. Keep light wavelength, pigment form and gene expression distinct.

During germination, gibberellin signalling stimulates aleurone cells to produce amylase. Amylase hydrolyses starch in the endosperm to soluble sugars that the embryo can respire and use for growth.

Compare germinating and non-germinating grains or vary a condition while controlling temperature, water and time. Measure reducing sugar or iodine-starch change with suitable repeats and controls.

A grain with active amylase loses the blue-black iodine colour as starch falls and gains soluble sugar; that sugar supports respiration rather than being “new starch”.

Iodine detects starch, not amylase directly, and a colour change needs a controlled comparison. Do not infer enzyme activity from germination alone.

Nervous control uses rapid electrical impulses and targeted neurotransmitter release; hormonal control uses chemicals carried in blood, usually with slower onset and longer-lasting, broader effects. Both use receptors, coordination centres and effectors.

A reflex can move a hand away quickly, while adrenaline or thyroxine changes metabolism across several tissues. The best system depends on speed, duration and distribution.

The systems can interact: neural signals can trigger hormone release, and hormones can alter the sensitivity or activity of nervous tissues.

Hormones do not always act slowly and nerves do not always produce a brief response. Compare route, target, timing and persistence rather than memorising a single slogan.

Brain regions specialise in tasks such as sensory processing, movement, coordination, memory and endocrine control, but behaviour emerges from networks rather than one isolated “on/off” centre.

A motor area can initiate movement while the cerebellum coordinates timing and the brainstem regulates vital functions; damage to one region can be partly compensated by connected circuits.

Functional evidence from lesions, imaging and stimulation must be interpreted with anatomy and task demands together.

A labelled brain map is not proof that one region alone causes a behaviour. Avoid deterministic localisation when the evidence shows distributed processing.

Brain imaging methods answer different questions: structural scans show anatomy, while functional methods track activity or blood flow during a task. The interpretation depends on timing, resolution and the comparison condition.

A region that is more active during a task may be involved without being the only cause. Converging evidence from lesions, stimulation and behaviour strengthens a localisation claim.

If a motor task increases activity in a cortical area compared with a matched rest condition, the result supports involvement; it does not prove that the area alone controls movement.

Correlation between activity and a task is not proof of a single function, and an image is not a diagnosis without clinical context.

Some disorders are associated with altered neurotransmitter levels or signalling. Parkinson’s involves reduced dopamine from lost neurones; antidepressant drugs can increase serotonin or noradrenaline signalling.

A drug may mimic a transmitter, supply a precursor, block breakdown or inhibit reuptake. These mechanisms change synaptic transmission, but symptoms usually involve networks and multiple contributing factors.

L-dopa is converted into dopamine in the brain, while an SSRI reduces serotonin reuptake so more remains in the synaptic cleft.

“Low neurotransmitter causes the disorder” is stronger than the evidence usually supports. Distinguish an association, a treatment mechanism and a complete explanation.

A desired gene is isolated, amplified and joined to a plasmid vector using restriction enzymes and ligase. The recombinant plasmid enters a microorganism, which is cultured in a fermenter to make the protein for purification.

Microbes grow rapidly and express the inserted gene at scale. The final product must still be isolated, purified and checked for safety and function.

A bacterial plasmid carrying the human insulin gene allows cultured bacteria to produce insulin, which is purified rather than administered with the whole bacterial culture.

A vector carries DNA but does not guarantee correct expression or a safe product. Separate gene insertion, culture, purification and quality control.

Recombinant DNA is formed when DNA from different sources is joined. A restriction enzyme cuts the desired gene and vector, complementary ends pair, and DNA ligase seals the sugar-phosphate backbone.

PCR can amplify the target before insertion, while a plasmid provides replication or expression signals in the host. The construct must be introduced into cells and selected or screened.

A gene coding for insulin can be joined to a bacterial plasmid; the plasmid is then transferred into bacteria where the gene may be expressed.

Cutting DNA is not the same as expressing it. A recombinant construct needs a compatible host, promoter and verification before useful protein is produced.

A recombinant plasmid or vector must enter a suitable host cell. Selection or screening distinguishes cells that received the construct, after which expression and product quality can be tested.

Transformation is only the entry step: culture conditions, selectable markers, gene orientation and host machinery affect whether the target protein is made.

A bacterial colony carrying the plasmid may grow on selective medium, but protein assays are still needed to show that the inserted gene is expressed correctly.

Antibiotic resistance as a marker does not prove therapeutic protein production, and a vector is not itself the finished medicine.

A microarray uses labelled nucleic acids from samples to measure which genes are expressed relative to a reference. Complementary binding at spots produces a pattern that can be compared between tissues or conditions.

The result is a relative expression profile, not a direct measurement of every protein or a guaranteed cause. Controls, normalisation and probe specificity determine how confidently differences can be interpreted.

A gene spot with stronger signal in diseased tissue suggests higher transcript abundance, but follow-up experiments are needed to test whether the gene drives the phenotype.

A microarray signal is not automatically protein activity, and a difference in expression is not proof of causation.

Bioinformatics uses databases and computational tools to compare DNA, RNA or protein sequences, predict relationships and identify patterns. The output depends on the input sequence, reference database and comparison method.

Check alignment quality, sequence length, conserved regions and the scoring or statistical assumptions before interpreting a match.

A high sequence similarity can support common ancestry or a shared function, while a low-quality or partial sequence may produce a misleading result.

A database hit is not proof of function or causation. Distinguish similarity, homology, prediction and experimental confirmation.

Genetic modification can add a useful characteristic, such as producing a medicine or resisting a pest. Its value depends on effectiveness, containment, ecological effects, ownership, welfare and who receives the benefit.

Benefits may include reliable therapeutic protein production or reduced losses; risks include unintended gene flow, resistance, ecological disruption and ethical objections to animal or food applications.

A GM microorganism making insulin is contained and purified, whereas a GM crop releasing a trait into wild relatives raises a different monitoring problem.

“GM” is not automatically safe or harmful. Judge the specific organism, gene, environment and evidence rather than using a blanket claim.