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At least 19 recordsLinked to original sources

Histochemical and cellular aspects of adipose tissue development in decapitated pig fetuses: an ontogeny study.

Adipose tissue from fetuses decapitated at 45 d of gestation was removed and structurally and histochemically analyzed at 65, 85 and 110 d of gestation. Subcutaneous adipose tissue from decapitated and control fetuses at 65 d of gestation was histologically and histochemically similar. A reduced number of fat cell clusters in the outer layer of subcutaneous tissue and a poorly developed dermis was evident in decapitated fetuses at 85 d of gestation. Fat cell size was similar for control and decapitated fetuses at 65 d of gestation, whereas cells in 85 d-old decapitated fetuses were larger than cells in control fetuses. Adipocytes from control and 85 d-old decapitated fetuses were histochemically similar except for an elevated number of esterase positive cells in decapitated fetuses. At 110 d of gestation, adipocytes from decapitated fetuses had higher activities of the following enzymes than did control adipocytes: malate dehydrogenase (NADP dependent) glucose 6-phosphate dehydrogenase NADP dependent), isocitrate dehydrogenase (NADP dependent), alpha-glycerol phosphate dehydrogenase (NADP dependent), NADPH-tetrazoleum reductase and esterase. Levels of succinate dehydrogenase, glutamate dehydrogenase and NADH-tetrazoleum reductase were similar in cells from controls and decapitated fetuses. These data indicate that fetal decapitation probably exerts a positive influence on enzymes involved in lipid synthesis. However, fetal decapitation also exerts a negative influence on fat cell hyperplasia.

Adipose Tissue↗

Euthanasia by decapitation: evidence that this technique produces prompt, painless unconsciousness in laboratory rodents.

Rapid euthanasia of laboratory rodents without the use of anesthesia is a necessary research technique whenever there is the likelihood of anesthesia or stress interfering with the chemistry of the tissues under investigation. Decapitation has long been the procedure of choice under such circumstances. Recently, however, the American Veterinary Medical Association (AVMA) panel on euthanasia recommended that decapitation be avoided on the grounds that the decapitated head may be conscious and suffering for as much as 15 seconds. The panel further recommended that if decapitation was scientifically necessary, the decapitated head be immediately immersed in liquid nitrogen. These AVMA guidelines now enjoy regulatory status; the recommendation that decapitation be avoided has thus caused considerable difficulty for all research requiring rapid, anesthesia-free collection of tissues. The scientific validity of these recommendations is consequently a matter of great practical as well as theoretical importance. The decision to discourage decapitation appears to have been based on a single literature report claiming that the EEG of the decapitated head revealed conscious suffering for more than 10 seconds (Mikeska and Klemm 1976). This review carefully examines the scientific literature on this subject. It is concluded that the report by Mikeska and Klemm of EEG activation in the decapitated head is correct, but that this phenomenon is also seen when the decapitated head is under deep anesthesia, and in normal brains under ether anesthesia or during REM sleep. Hence these findings do not demonstrate either consciousness or the perception of pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Welfare↗

Effects of stunning and decapitation on broiler activity during bleeding, blood loss, carcass, and breast meat quality.

Four experiments were conducted to determine the effects of electrical stunning and decapitation on bird activity as well as carcass and meat quality. In Experiment 1, broilers were subjected to one of four stunning and killing methods: no stun and neck cut, stun and neck cut, no stun and decapitation, and stun and decapitation. Birds were scored for severity of physical activity on a scale of 1 to 4 with 1 being no activity and 4 being severe wing flapping and muscular contractions. Carcasses were also scored for red wing tips and broken bones. In Experiments 2 to 4, all birds were stunned prior to neck cut or decapitation. Carcasses were scored as described in Experiment 1 as well as measurements of blood loss, feather removal, and breast meat pH, color, cook loss, and tenderness. Based on carcass activity in Experiment 1, decapitation following stunning was similar to a conventional stun and unilateral neck cut, except there was almost no late activity (after 60 s) observed in the decapitated birds. Decapitation following stunning did not result in any consistent carcass quality defects compared to conventional killing in the four experiments. No differences were found in 24-h lightness values, yellowness, cook yield, tenderness, and ultimate pH between conventionally killed and decapitated birds. Blood loss and breast meat redness were inconsistent. These results indicate that high frequency stunning and decapitation may be an acceptable alternative to conventional slaughter based on carcass and meat quality and by ensuring an irreversible loss of consciousness.

Abattoirs↗

Changes after Decapitation in Concentrations of Indole-3-Acetic Acid and Abscisic Acid in the Larger Axillary Bud of Phaseolus vulgaris L. cv Tender Green.

Early changes in the concentrations of indole-3-acetic acid (IAA) and abscisic acid (ABA) were investigated in the larger axillary bud of 2-week-old Phaseolus vulgaris L. cv Tender Green seedlings after removal of the dominant apical bud. Concentrations of these two hormones were measured at 4, 6, 8, 12 and 24 hours following decapitation of the apical bud and its subtending shoot. Quantitations were accomplished using either gas chromatography-mass spectrometry-selected ion monitoring (GS-MS-SIM) with [(13)C(6)]-IAA or [(2)H(6)]-ABA as quantitative internal standards, or by an indirect enzyme-linked immunosorbent assay, validated by GC-MS-SIM. Within 4 hours after decapitation the IAA concentration in the axillary bud had increased fivefold, remaining relatively constant thereafter. The concentration of ABA in axillary buds of decapitated plants was 30 to 70% lower than for buds of intact plants from 4 to 24 hours following decapitation. Fresh weight of buds on decapitated plants had increased by 8 hours after decapitation and this increase was even more prominent by 24 hours. Anatomical assessment of the larger axillary buds at 0, 8, and 24 hours following decapitation showed that most of the growth was due to cell expansion, especially in the intermodal region. Thus, IAA concentration in the axillary bud increases appreciably within a very few hours of decapitation. Coincidental with the rise in IAA concentration is a modest, but significant reduction in ABA concentration in these axillary buds after decapitation.

Journal Article↗

Morphological development of the thyroid gland and serum T4-concentration in the intact and decapitated pig fetus.

The morphological and functional development of the fetal pig thyroid gland between 50 and 110 days post coitum have been examined in the normal pig fetus and after fetal decapitation at 42 days postcoitum. Body length and body weight developed at the same rate, comparing control and decapitated animals. Thyroid gland weight increased between 50 days and 110 days from 1.3 +/- 0.5 mg (SD) to 130.0 +/- 35.0 mg in control fetuses and from 0.9 +/- 0.2 mg to 113.4 +/- 23.0 mg in decapitated fetuses. A number of histomorphometrical parameters in thyroid tissue were measured. No significant differences in follicular epithelial height were observed between decapitated and control animals at 75 and 110 days. In control animals follicles increased both in size and number. In decapitated animals the follicles increased strikingly in number, but only slightly in size. Although colloid was formed in glands of decapitated animals, it was much less than in control fetuses. The gland of decapitated animals of 110 days resembled histologically the gland of much younger control animals (60 to 75 days). Gland development after fetal decapitation at 42 days may represent autonomous development when Thyroid Stimulating Hormone (TSH) is depleted. Serum thyroxine concentration (T4) was determined by radioimmunoassay and increased in control animals from 0.06 +/- 0.01 micrograms/100 ml to 4.18 +/- 0.87 micrograms/100 ml at 110 days, the greatest rate of increase being observed between 64 and 90 days. In decapitated fetuses serum T4 remained very low, namely less than 0.20 micrograms/100 ml. It is very unlikely that any significant transfer of T4 from mother to fetus or from one fetus to another occurred. Both the rise in serum T4 and the enlargement of the follicles may be TSH dependent events in fetal pig thyroid gland development, whereby the sudden rise is serum T4 precedes the greatest rate of increase in follicle size.

Animals↗

Effect of decapitation and ACTH on somatic development of the rabbit fetus.

Rabbit fetuses were decapitated, injected with ACTH or decapitated and injected with ACTH on day 24 of gestation. On day 29 the body weight and weight of the interscapular fat pad were compared with those of littermates. The weight, total DNA and weight/DNA ratio of the liver, heart and kidney were measured in experimental and control fetuses. A comparison was made between decapitated and control fetuses of the length of the hind limb bones and number of ossified vertebrae. The body weight of the decapitated or ACTH-injected fetus ranked significantly below the mean for the litter, but decapitated fetuses injected with ACTH ranked close to the litter mean. The growth retardation of the decapitated fetus was not manifest in the kidneys which were heavier and had a greater number of cells than normal, nor in the cell size of the heart, liver or kidneys which were equal to those of the heaviest fetus in the litter. Decapitation had no specific effect on ossification. Growth retardation of the ACTH-injected fetus was mirrored by different patterns of DNA and weight/DNA reduction in the three organs studied. Decapitation retards growth in body weight of the fetal rabbit which may be corrected by ACTH. It is concluded that the hypophyseal-adrenal axis plays a role in the control of normal fetal growth but that excess secretion of glucocorticoids results in stunting.

Adrenocorticotropic Hormone↗

Effect of fetal decapitation on the composition and metabolic characteristics of pig skeletal muscle.

The effect of fetal decapitation on the compositional and metabolic characteristics of the biceps femoris muscle of the pig was studied. Fetuses were decapitated at 45 days of gestation and sampled at 110 days of gestation. Muscle wet weight was greater and total dry matter was lower in decapitated (D) than in control (C) fetuses. Total muscle triglyceride content was not influenced by decapitation, but the triglyceride concentration was lower in D when compared to C fetuses. Muscle cell number (total muscle DNA) was not influenced by decapitation, but protein/DNA was greater in the muscle of D than C fetuses. Aerobic metabolism, as measured by oxidation of pyruvate, isoleucine, and palmitate to CO2, was not influenced by decapitation. The rate of palmitate esterified and the ratio of palmitate oxidized/esterified was normal in decapitated fetuses. While the tricarboxylic acid cycle appeared to function normally, pentose shunt activity was higher in the decapitated fetal muscle than in control muscle. Although the rate of decarboxylation of leucine was lower in the muscle of D than in C fetuses, the net rate of leucine transaminated was similar between C and D fetuses.

Amino Acids↗

Dynamic development of Trypanosoma cruzi in Rhodnius prolixus: role of decapitation and ecdysone therapy.

Decapitation and ecdysone therapy on the population dynamics of the Trypanosoma cruzi Dm28c clone in the stomach, small intestine and rectum of fifth-instar larvae of Rhodnius prolixus were investigated. Parasites were not found in the small intestine and rectum of decapitated insects after 10 days post-infection (p.i.). Decapitated ecdysone-supplemented insects sustained the flagellate infection in both gut compartments. In the rectum, the population density of parasites increased 5-fold in ecdysone-treated decapitated larvae and 7-fold in control insects. Epimastigote forms dominated with 40-65%, intermediate stages and round forms varied over 10-35% in the stomach, small intestine and rectum in both insect groups. Low numbers of metacyclic trypomastigotes were observed in the stomach and small intestine of the control group and decapitated insects supplemented with ecdysone but, at 15 days p.i., this form of flagellate reached about 20% in the rectum of the control insects. In the entire gut, at 30 days p.i., 23% of parasites in the control group and 8% in the decapitated insects treated with ecdysone were found. These results indicate that a head factor, possibly the prothoracicotropic hormone from the brain which stimulates ecdysone production by the prothoracic glands, may act directly or indirectly to stimulate the development of epimastigotes and round forms of the parasite and that a single ecdysone treatment is not able to fully reverse metacyclogenesis in decapitated R. prolixus.

Animals↗

The role of locus coeruleus in decapitation convulsions of rats.

The role of the central norepinephrine (NE) system, especially the locus coeruleus (LC), in the occurrence of decapitation convulsions was investigated in rats. Intraspinal injection of 6-hydroxydopamine (6-OHDA) caused a significant inhibition of decapitation convulsions as shown by prolongation of the latency and shortening of the convulsion's duration, as well as decreasing the NE content of the spinal cord to 35% of the control value without affecting the NE content of the various regions in the brain. Chemical lesion of the descending bundle from the LC by treatment with 6-OHDA significantly inhibited decapitation convulsions in a similar manner. Moreover, there was a decrease in the NE content of the spinal cord and hypothalamus to 24% and 47% of the control value, respectively. Bilateral electrolytic lesion of the LC also significantly inhibited decapitation convulsions and decreased the NE content of the cortex and spinal cord to 15% and 74% of the control value, respectively. However, lesions of the dorsal and ventral NE bundle by treatment with 6-OHDA, which caused a marked decrease in the NE content of the cortex and hypothalamus, respectively, did not affect the decapitation convulsion. Intraspinal injection of 5,6-dihydroxytryptamine resulted in a decrease in the 5-hydroxytryptamine content of the spinal cord only; moreover, it did not change the decapitation convulsion. These results suggest that coeruleospinal NE neurons play an important role in the occurrence of decapitation convulsions.

5,6-Dihydroxytryptamine↗

Metabolism of inositol 1,4,5-trisphosphate in mouse brain due to decapitation ischemic insult: effects of acute lithium administration and temporal relationship to diacylglycerols, free fatty acids and energy metabolites.

Previous studies have shown that global cerebral ischemia induced by decapitation leads to the stimulated hydrolysis of poly-phosphoinositides. In this study, the decapitation model was used to further examine the temporal events related to metabolism of Ins(1,4,5)P3 and the release of diacylglycerols (DGs) and free fatty acids (FFAs) in the mouse brain. Since lithium administration is known to inhibit inositol monophosphatase activity in brain, the effects of acute lithium injection on Ins(1,4,5)P3 metabolism were also examined. Cerebral ischemia induced by decapitation of C57 Bl/6J mice resulted in transient increases of Ins(1,4,5)P3, Ins(1,4)P2 and Ins(4)P which peaked at 35, 65 and 125 s, respectively. The level of Ins(1)P, however, was not altered. Mice administered lithium by intraperitoneal injection (8 meq/kg for 4 h) gave rise to a 40- and 4-fold increase in levels of Ins(1)P, Ins(4)P, respectively, a 20% increase in levels of Ins(1,4)P2 but no apparent changes in the levels of Ins(1,4,5)P3. Decapitation also induced an increase in the levels of DGs and FFAs. Unlike the transient appearance of Ins(1,4,5)P3, however, DG levels increased steadily for 2 min and then reached a plateau whereas the FFAs showed a lag time of 35 s prior to a biphasic increase. During the initial 2 min after decapitation, there was a preferential increase in the DG species containing 18:0 and 20:4. Lithium administration did not alter the decapitation-induced release of DG and FFA. As expected, decapitation gave rise to a rapid decrease in the levels of phosphocreatine and ATP and the decline in ATP was marked by a transient appearance of ADP and a concomitant increase in AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pathologic features of suicidal complete decapitations.

Despite high suicide rates all over the world, complete decapitation as a consequence of violent suicide methods is exceptionally rare and there is always a potential for confusion with homicide as well as with body dismemberment or mutilation. We analyzed the phenomenology and morphology of 10 cases (six male, four female; individual age 18-60 years) of suicidal complete decapitation that were subjected to medico-legal autopsies at the Institute of Legal Medicine, University of Hamburg, Germany, between 1995 and 2002. All decapitations occurred while the person was alive as proven by signs of vitality. Blood alcohol levels were positive in five cases and ranged between 28 and 202 mg/dl. The applied methods of suicide were running over by a train in eight cases and hanging in two cases. In suicidal hanging resulting in complete decapitation the wound margins were clear-cut with an adjacent sharply demarcated circumferential band-like abrasion zone showing a homogenous width, the latter determined by the thickness of the rope. In decapitations due to railway interference a broad spectrum of pathologic alterations such as the co-existence of irregular, ragged and sharp-edged wound margins, vascular and nervous pathways forming bridges in the depth of the wound and bruising could be observed. In such cases skin abrasion zones were generally not circumferential and showed a heterogenous width. Concerning hanging-related complete decapitations, our findings are well in line with those of other authors, namely that heavy body weight of the suicidal, fall from a great height and in some cases inelastic and/or thin rope material used for the noose are the determining factors decisive for complete decapitation.

Adolescent↗

Ovarian development in control and decapitated pig fetuses.

Ovarian development was studied in control and decapitated pig fetuses. Fetuses were decapitated at 42 days postcoitum. At 51, 61, 74, 90 and 112 days postcoitum decapitated and control females were collected. Ovarian weight gradually increased during development in control animals. Deprivation of pituitary hormones as a result of fetal decapitation did not cause a decline in ovarian weight increase. Germ cell maturation in control and decapitated fetuses proceeded in a similar fashion, with secondary follicles being the most advanced stage. Enzyme histochemical activity was present in the primary interstitial gland cells and in granulosa cells and was similar in normal and decapitated fetuses. Both NADH diaphorase activity and 3 beta-hydroxysteroid dehydrogenase activity increased from 51 to 74 days and remained relatively constant thereafter. Since fetal decapitation in the pig hardly influences ovarian development, pituitary dependency of the fetal ovary in the pig is unlikely.

3-Hydroxysteroid Dehydrogenases↗

Regulation of rabbit fetal glycogen: effect of in utero fetal decapitation on the metabolism of glycogen in fetal heart, lung, and liver.

To understand the control mechanisms involved in the regulation of fetal glycogen, we have studied the effect of in utero fetal decapitations on glycogen metabolism in rabbit fetal heart, lung, and liver. In utero fetal decapitations were performed between days 18 and 21 of gestation. Two to four fetuses on one side of the horn were decapitated. Fetuses were delivered between days 23 and 26 or between days 28 and 30 of gestation. Fetal heart, lungs, and liver were analyzed for DNA, protein, glycogen, glycogen synthase (I and D forms), glycogen phosphorylase (a and b forms), phosphofructokinase, pyruvate kinase, and lactic dehydrogenase. In fetal heart and lung, no difference was observed in any of the above measurements in the intact and decapitated fetuses. In contrast, fetal liver does not appear to develop the glycogen system as indicated by the very low levels of glycogen (0.02 mg/mg DNA) in decapitated fetuses as compared with intact fetuses (0.4 mg/mg DNA). Similarly the levels of glycogen synthase and phosphorylase were two to three times lower in livers from decapitated fetuses as compared with the livers from intact fetuses. The three enzymes phosphofructokinase, pyruvate kinase, and lactic dehydrogenase were not affected by fetal decapitation in all three tissues. These results indicate that the fetal hypothalamic-pituitary-adrenal (thyroid) axis is not required at least after day 18 of gestation for the normal accumulation and subsequent utilization of glycogen in fetal heart and lungs, while it is an absolute requirement for the development of the fetal liver glycogen system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Decapitation impacting effect of topically applied chlorpyrifos on acetylcholinesterase and general esterases in susceptible and resistant German cockroaches (Dictyoptera: Blattellidae).

The effect of topically applied chlorpyrifos on acetylcholinesterase and other esterases in heads and decapitated bodies of CSMA and Crawford German cockroaches was examined with spectrophotometric enzyme assay and native polyacrylamide gel electrophoresis. The toxicity of chlorpyrifos was greatly reduced in decapitated CSMA male cockroaches with LD50 value 17.1-fold higher than that of normal CSMA cockroaches. Acetylcholinesterase activity from heads was significantly higher in the Crawford compared with the CSMA strain and did not change until 24 h after chlorpyrifos in vivo treatment in both strains. The p-nitrophenyl butyrate (NPB) esterase activities from both heads and decapitated bodies of the resistant Crawford strain were significantly greater than the susceptible CSMA strain. The p-NPB esterase activity was significantly inhibited by chlorpyrifos in vivo treatment, and total p-NPB esterase activity was significantly reduced in decapitated bodies compared with heads of both strains. Native polyacrylamide gel electrophoresis (PAGE) analysis of extracts solubilized with Triton X-100 from heads and decapitated bodies revealed five major esterase bands and an acetylcholinesterase (AChE) band with a high capability of hydrolyzing alpha-naphthyl butyrate and acetylthiocholine, respectively. In the heads of susceptible CSMA male cockroaches, the activity of mobile isozymes d1 and d2 was completely inhibited at 24 h after chlorpyrifos application, and isozyme e was partially inhibited. In contrast, isozymes c1 and c2 from the decapitated bodies of CSMA cockroaches were mostly affected at 24 h after the topical application of chlorpyrifos. The activities of acetylcholinesterase and esterase isozymes a and b from the decapitated body remained uninhibited in both strains. Inhibition of isozymes d1 and d2 seems to be more important in chlorpyrifos intoxication than acetylcholinesterase.

Acetylcholinesterase↗

Effect of decapitation and chronic in-vivo treatment with a gonadotrophin-releasing hormone agonist on testicular steroidogenesis in the rat fetus.

To study the effect of in-vivo gonadotrophin-releasing hormone (GnRH) treatment on testicular testosterone production during late fetal life in the rat, 18.5-, or 20.5-day-old fetuses were decapitated and injected with either long-acting microcapsules containing the GnRH agonist D-Trp-6-GnRH or vehicle only. Two days later, fetal and maternal plasma was collected and fetal testes were removed and incubated for 6 h in medium with either 100 ng LH/ml or without LH. The GnRH agonist concentrations in the plasma of GnRH-treated decapitated male fetuses were comparable in the two age-related groups (5 nmol/l). After treatment of the fetus with D-Trp-6-GnRH, the agonist was recovered in maternal plasma, showing that this peptide can cross the fetal-maternal barrier. In 22.5-day-old decapitated vehicle-treated male fetuses, the plasma testosterone level dropped to that observed in control female fetuses, and treatment of decapitated male fetuses with the GnRH agonist did not further reduce it. At both days 20.5 and 22.5, basal in-vitro testosterone secretion by testes from decapitated vehicle-treated fetuses was lower than secretion by testes from intact control fetuses from the same litter, but LH-stimulated secretion was similar in both groups. Both basal and LH-stimulated secretion by testes from GnRH-treated decapitated fetuses was lower than secretion by testes from vehicle-treated decapitated fetuses and larger reductions were measured on day 22.5 than on day 20.5 (-48 vs -18% for basal secretion, and -76 vs -40% for LH-stimulated secretion).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum hormones and metabolites in fetally decapitated pigs.

The effects of fetal decapitation on serum hormones and metabolites were studied in utero in the pig. Pig fetuses were decapitated at 45 days of gestation and serum sampled from the umbilical vein and artery of each fetus and from the uterine artery at 110 days of gestation. Serum levels of cortisol were reduced in decapitated fetuses when compared to intact controls. The data suggest that the decapitated fetus derived its cortisol primarily from maternal sources. Decapitation produced a deficiency of serum RIA growth hormone, T3 and T4. The absence of these hormones produced no effect on fetal growth. Serum insulin, glucagon and triglycerides were elevated in decapitated fetuses. Arterial venous differences in blood glucose indicated that the decapitated fetuses were utilizing glucose at a higher rate than intact fetuses. The alterations seen in serum insulin and triglycerides suggest that neural mechanism may be involved in prenatal lipid deposition.

Animals↗

Acidic phospholipids, diacylglycerols, and free fatty acids in gerbil brain: a comparison of ischemic changes resulting from carotid ligation and decapitation.

The levels of brain acidic phospholipids (poly-PI, PI, PA, and PS), DG, and FFA and their acyl group profiles were determined after induction of ischemia in gerbils by ligation of the common carotid arteries and decapitation. Ischemia induced by both procedures resulted in a significant decrease in poly-PI (20% for 1-min decapitation and 1-min ligation). Except for a 16% increase in PI in the 5-min decapitation group, no apparent change was found in other phospholipids after either ischemic condition. The level of DG was increased one- and three-fold after 1 and 5 min, respectively, of decapitative ischemic treatment. Ligation of the carotid arteries for 1 min resulted also in a one-fold increase in the DG level. The decapitative model resulted in a one- and five-fold increase in FFA level (with respect to 1 and 5 min, respectively), whereas ligation for 1 min resulted in an increase of 42% of the FFA. The acyl groups of poly-PI and PI in the control gerbil brain are enriched in 18:0 and 20:4, but those of DG, FFA, and PA have a higher proportion of 16:0 besides 18:0 and 20:4. However, a preferential increase in the proportion of 18:0 and 20:4 was shown for the DG and FFA in both types of ischemic treatments. It is concluded from the results that both models of ischemic treatment elicit a similar decrease in poly-PI and increase in DG, but differ in the amount of FFA release. The higher level of FFA release in the decapitative model suggests that other biochemical mechanisms may be activated to cause the additional release.

Animals↗

The Distance to Which Wound Effects Influence the Structure of Secondary Xylem of Decapitated Pinus pinea.

Decapitation of stems of annuals and trees for the study of vascular and fiber differentiation with or without hormonal application is a common procedure. There is controversy about whether wound effects play a role in such experiments, and to what distance from the point of decapitation. To examine this question, the distance from the point of decapitation at which apparent wound effects are obvious developmentally, was studied in decapitated 4-year-old Pinus pinea plants. The wound effects just below the cut included differentiation of many traumatic resin ducts, a parenchyma band instead of tracheids, more tracheid files, and a higher proportion of late wood. The increase in the number of resin ducts was still considerable and statistically significant 10 cm below the point of decapitation compared with the nondecapitated control. These results indicate that in pines, wound effects in the first 5 cm below the decapitation point (a common point for tissue examination) cannot be ignored in experiments on the regulation of vascular differentiation.

Journal Article↗