Recovery potential of black rockfish, Sebastes melanops Girard, recompressed following barotrauma.

Overfished species of rockfish, Sebastes spp., from the Northeast Pacific experience high bycatch mortality because of 'barotrauma', a condition induced from the rapid change in pressure during capture. Field experiments show that it may be possible for rockfish to recover from barotrauma if quickly recompressed; however, no work has followed the physiological recovery of rockfish after recompression or determined whether it is possible for rockfish to survive barotrauma in the long term. Barotrauma was induced in adult black rockfish, Sebastes melanops Girard, from a simulated depth of 35 m, followed by recompression. Blood and selected tissues (eye, heart ventricle, head kidney, liver, rete mirabile and gonad) were sampled at days 3, 15 and 31 post-recompression to evaluate the tissue- and physiologic-level response during recovery. No mortality from barotrauma occurred during the experiments, and feeding resumed in 80% of both treatment and control fish. The primary injury in treatment fish was the presence of a ruptured swimbladder and/or a ruptured tunica externa (outer layer of swimbladder), which was slow to heal. Blood plasma was analysed for glucose, sodium, chloride, potassium, calcium, phosphorus, insulin-like growth factor-1 and cortisol. Plasma analyses indicated no strong effects because of barotrauma, suggesting overall handling stress outweighed any effect from barotrauma. Rockfish with ruptured swimbladders may face compromised competency in the wild; however, it appears the majority of black rockfish decompressed from 35 m have a high potential for recovery if recompressed immediately after capture. This research suggests recompression could be a valuable bycatch mortality reduction tool for rockfish in recreational fisheries.

Corn oil intake favorably impacts lipoprotein cholesterol, apolipoprotein and lipoprotein particle levels compared with extra-virgin olive oil.

BACKGROUND: Corn oil (CO) and extra-virgin olive oil (EVOO) are rich sources of unsaturated fatty acids (UFA), but UFA profiles differ among oils, which may affect lipoprotein levels. OBJECTIVES: The objective of this study was to assess the effects of CO versus EVOO intake on fasting lipoprotein and subfraction cholesterol levels, apolipoprotein (apo) A1, apo B, and low-density lipoprotein particle concentrations in men and women. SUBJECTS/METHODS: As part of a weight maintenance diet, men and women were provided with food items prepared with 54 g per day of CO or EVOO (21-day treatment, 21-day washout) in a randomized, double-blind, controlled-feeding, crossover trial. Fasting lipoprotein cholesterol and related variables were determined with density gradient ultracentrifugation. RESULTS: Among the 54 completers, CO reduced total cholesterol, low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), apo B and LDL particle concentration to a greater extent compared with EVOO intake. Changes in LDL-C and VLDL-C contributed to the larger reduction in non-HDL-C with CO compared with EVOO intake (-0.39 mmol/l vs -0.04 mmol/l; P<0.001). The larger reduction in LDL-C by CO intake was attributable to changes (P<0.05) caused by CO vs EVOO in large LDL1+2-C (-0.22 mmol/l) and intermediate-density lipoprotein cholesterol (-0.12 mmol/l). HDL-C responses did not differ between treatments, but apo A1 increased more with EVOO compared with CO intake (4.6 versus 0.7 mg/dl, respectively, P=0.016). CONCLUSIONS: CO intake reduced atherogenic lipoprotein cholesterol and particle concentrations to a larger extent than did EVOO, which may have implications for cardiovascular disease risk.

Insulin-like growth factor binding protein 3 mediates retinoic acid- and transforming growth factor beta2-induced growth inhibition in human breast cancer cells.

Retinoic acid (RA) is a potent in vitro inhibitor of cell proliferation in various malignant cell lines. The exact mechanisms of its actions, however, are not fully understood. To further elucidate the nature of this inhibition, we investigated the effects of RA in an estrogen receptor-negative human breast cancer cell line, MDA-MB-231. RA (0.01-5 microM) significantly inhibited MDA-MB-231 cell growth by 35-40% as compared with untreated controls. Similar growth inhibitory actions were observed when cells were treated with transforming growth factor beta2 (TGF-beta2), another factor with antiproliferative actions in breast cancer cells. Both RA and TGF-beta2 increased the levels of insulin-like growth factor binding protein (IGFBP) 3 (2-3-fold) and mRNA (1.5-2-fold), whereas IGFBP-4 levels remained essentially unchanged. The direct involvement of IGFBP-3 in cell growth inhibition was further confirmed by its action on cell growth: exogenous IGFBP-3 directly and significantly inhibited MDA-MB-231 cell number by 40%. These results provided circumstantial evidence that IGFBP-3 may mediate RA and TGF-beta2 growth inhibitory actions in human breast cancer cells. To test this hypothesis, we used an antisense IGFBP-3 oligodeoxynucleotide (ODN) which specifically inhibits IGFBP-3 expression. The antisense IGBP-3 ODN dramatically blocked both RA- and TGF-beta2-induced increases in IGFBP-3 protein (90%) and mRNA levels (90%). This effect was not observed when RA- or TGF-beta2-exposed cells were treated with sense IGFBP-3 ODN. Moreover, antisense ODN did not significantly affect IGFBP-4 protein or mRNA levels, strongly supporting the specificity of the antisense IGFBP-3 ODN effect on IGFBP-3 mRNA. This specific effect of antisense IGFBP-3 ODN on IGFBP-3 protein and mRNA levels was accompanied by significant attenuation of the inhibition of cell proliferation attained with RA or TGF-beta2 (approximately 40% of either RA- or TGF-beta2-induced inhibition). The control sense IGFBP-3 ODN did not reduce the growth inhibition observed with either RA or TGF-beta2. These results indicate that IGFBP-3 is an important mediator of RA- and TGF-beta2-induced cell growth inhibition in human breast cancer cells.

An insulin-like growth factor I-resistant state in cartilage of diabetic rats is ameliorated by hypophysectomy. Possible role of metabolism.

This study investigated the effect of IDDM on cartilage anabolic activity in rats. Rats were injected with STZ to induce IDDM, were hypophysectomized, or were injected with STZ and hypophysectomized. After 14 days, control (intact and sham-Hx) and Hx rats were normoglycemic, whereas the rats with IDDM exhibited hyperglycemia and glycosuria. The HxDb rats, however, had normal blood glucose levels and no glycosuria. Both growth, serum levels of IGF-I, and basal cartilage 35SO4 incorporation measured in vitro were decreased in the Hx, IDDM, and HxDb groups. IGF-I added in vitro significantly stimulated 35SO4 incorporation by cartilage explants from control and Hx animals, whereas explants from the animals with IDDM were unresponsive. Explants from the HxDb rats, however, were stimulated by IGF-I in a dose-related manner. Because Hx corrected the glycemic status of the IDDM rats and restored cartilage responsiveness to IGF-I, a second set of experiments was undertaken to further investigate the relationship between cellular metabolism and anabolic activity in cartilage. Cartilage explants from rats fasted for 48 h showed significantly decreased basal 35SO4 incorporation, which was as low as that in explants from rats with severe IDDM. Whereas explants from the IDDM rats were completely unresponsive, those from the fasted rats (and fed rats) were significantly stimulated by the added IGF-I. However, incubation in the presence of 2-D-G, which causes intracellular glucopenia, or in the absence of glucose, completely blocked the anabolic response to IGF-I in otherwise responsive tissues. In conclusion, an important component of diabetic growth inhibition appears to be tissue resistance to the anabolic action of IGF-I, a condition that is correctable by Hx and that may be a result of metabolic impairment at the tissue level.

Postnatal atresia of extraparenchymal pulmonary veins, fulminant necrotizing pulmonary arteritis and elevated circulating immune complexes.

An infant with operatively corrected total anomalous pulmonary venous connection developed postnatal atresia of the extraparenchymal left pulmonary veins with secondary arteritis of the ipsilateral intraparenchymal pulmonary arteries. Atresia of the right or left main pulmonary veins or of the common pulmonary vein is a rare occurrence and it is believed that association of such with necrotizing pulmonary arteritis has never been reported. This case illustrates the potential consequences of severe pulmonary venous obstruction in the absence of a left to right shunt.

Insulin-like growth factor-binding proteins (IGFBPs) and their regulatory dynamics.

The IGFBPs are a family of homologous proteins that have co-evolved with the IGFs and that confer upon the IGF regulatory system both functional and tissue specificity. IGFBPs are not merely carrier proteins for IGFs, but hold a central position in IGF ligand-receptor interactions through influences on both the bioavailability and distribution of IGFs in the extracellular environment. In addition, IGFBPs appear to have intrinsic biological activity independent of IGFs. The current status of research on IGFBPs is reviewed herein. Following a brief introduction to the entire IGF/IGFBP system, separate sections for each of the six cloned mammalian IGFBPs, the most extensive for IGFBP3, cover selected topics that emphasize the dynamics of IGFBPs--that is, their regulation in cells, their functionally important post-translational modifications, and their interactions in the cellular microenvironment--and how these dynamics influence physiological function.

Experimental diabetes mellitus in a teleost fish. I. Effect of complete isletectomy and subsequent hormonal treatment on metabolism in the goby, Gillichthys mirabilis.

The anatomical feature of a single pancreatic endocrine (islet) organ devoid of exocrine tissues and separated from other vital organs in the goby, Gillichthys mirabilis, allowed a relatively simple surgical isletectomy to be performed. Isletectomized (Ix) fish were then evaluated to determine whether the lack of islet hormones would cause the development of symptoms of insulin-dependent diabetes mellitus (IDDM) in a teleost fish. Isletectomy resulted in several symptoms typical of untreated IDDM in mammals. Plasma glucose was 3.5-fold higher in Ix animals (approximately 23 mmol/liter) than in intact and sham-Ix controls (6-7 mmol/liter), while urinary glucose was increased from less than 4 mmol/liter in controls to greater than 40 mmol/liter in Ix animals. Isletectomy also resulted in a significant elevation of plasma beta-hydroxybutyrate (from 0.7-0.8 to 1.0 mmol/liter). The severity of the metabolite imbalances was directly correlated with the degree of food consumption in Ix individuals, suggesting a reduced ability to assimilate dietary nutrients. In addition, distension of the abdomen due to increased food intake and a marked swelling of the urinary bladder suggested hyperphagia and polyuria, respectively, in the Ix animals. Insulin replacement therapy over 2 weeks corrected the glycosuria, polyuria, and hyperphagia and resulted in dose-related reductions in plasma glucose and beta-hydroxybutyrate levels. Injection of Ix animals with GH, on the other hand, produced no significant changes in any of the metabolic parameters measured. The establishment of this unique model of IDDM in an ectothermic vertebrate should prove valuable for future comparative studies on the role of insulin and other pancreatic factors in the regulation of metabolic and growth processes.

Experimental diabetes mellitus in a teleost fish. II. Roles of insulin, growth hormone (GH), insulin-like growth factor-I, and hepatic GH receptors in diabetic growth inhibition in the goby, Gillichthys mirabilis.

Insulin-dependent diabetes mellitus (IDDM), when untreated or poorly controlled in mammals, results in growth retardation. To determine whether the same relationship exists in an ectothermic vertebrate, IDDM-like symptoms were induced in a teleost fish, the goby Gillichthys mirabilis, by surgical removal of its pancreatic endocrine (islet) organ. Isletectomized (Ix) gobies lost body weight, their skeletal growth was retarded, as measured by changes in body length, and they exhibited a 50% reduction in cartilage 35SO4 incorporation in vitro, consistent with changes that occur in mammals with IDDM. Injections of bovine insulin into the Ix fish restored body growth parameters to control levels and stimulated cartilage 35SO4 incorporation in a dose-related manner. In contrast to mammals with IDDM, which are resistant to GH action, injection of teleost GH stimulated cartilage 35SO4 incorporation in the Ix fish. Furthermore, whereas cartilage from rats with IDDM is resistant to stimulation by insulin-like growth factor-I (IGF-I) in vitro, cartilage explants from the Ix fish were highly responsive to recombinant bovine IGF-I, exhibiting a dose-dependent stimulation of 35SO4 incorporation. As far as we are aware, these results represent the first demonstration of diabetic growth inhibition in an ectothermic vertebrate. This inhibition is similar to that which occurs in mammals with IDDM in some respects, but is different in others, as the diabetic fish did not develop resistance to growth stimulation by either GH or IGF-I. While these results support a role for insulin in maintaining the GH-IGF-I-growth axis in this ectothermic vertebrate, there may be important differences in the role of insulin in the promotion of anabolic processes.

Evidence for insulin-like growth factor (IGF)-independent transcriptional regulation of IGF binding protein-3 by growth hormone in SKHEP-1 human hepatocarcinoma cells.

Insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) is a polypeptide that forms a ternary complex with IGFs and an acid-labile subunit. The hormonal regulation of the components of this complex is highly controversial, and both IGF-I and GH have been shown to mediate the expression/synthesis of IGFBP-3. This study investigates the regulation of IGFBP-3 protein, measured by RIA and Western ligand blot, and messenger RNA (mRNA) expression, measured by Northern analysis and reverse transcriptase-PCR, in SKHEP-1 human hepatocarcinoma cells. SKHEP-1 cells significantly increased the IGFBP-3 concentrations in conditioned medium (CM) when treated with GH (0.1-10 ng/ml), IGF-I (1-100 ng/ml), or Des(1-3)-IGF-I (1-100 ng/ml) in a dose-dependent manner (>3-fold). The increase in IGFBP-3 protein concentrations in CM was accompanied by a corresponding increase in IGFBP-3 mRNA levels. Interestingly, time-course studies showed that the GH-induced increase in IGFBP-3 mRNA preceded the IGF-I-induced increase (6 h for GH-induced IGFBP-3 mRNA; 12 h for IGF-I-induced IGFBP-3 mRNA). The half-life of IGFBP-3 mRNA was evaluated after transcriptional arrest by treatment with a RNA polymerase II inhibitor (5,6-dichloro-1beta-D-ribofuranosylbenzimidazole), and was found to be 14-18 h and unaltered by GH or IGF-I treatment. The induction of IGFBP-3 by GH was not due to the indirect action of locally synthesized IGF-I, because 1) no immunoreactive IGF-I was detected in the CM of control or GH-treated cells; 2) Northern blots revealed no IGF-I mRNA expression in SKHEP-1 cells; 3) reverse transcriptase-PCR did not detect any expression of the IGF-I gene; and 4) time-course studies showed an earlier increase in IGFBP-3 mRNA after GH treatment than after IGF-I treatment. Thus, the results obtained in this study are consistent with an IGF-I-independent regulation of IGFBP-3 gene expression by GH.

Growth regulation in the gobiid teleost, Gillichthys mirabilis: roles of growth hormone, hepatic growth hormone receptors and insulin-like growth factor-I.

Studies of the teleost Gillichthys mirabilis were undertaken to assess the role of GH in regulating hepatic GH receptors, insulin-like growth factor-I (IGF-I) activity and cartilage growth. Hypophysectomized G. mirabilis were injected with saline vehicle or with 10, 100 or 1000 ng tilapia GH (tGH)/g every other day for 2-3 weeks. Growth, judged by increased body weight and length, was inhibited by hypophysectomy and stimulated by increasing tGH doses. Hepatic GH receptors, measured by 125I-labelled tGH binding, were decreased 50% by hypophysectomy. An additional dose-dependent reduction in binding was observed 24 h after tGH injection, but MgCl2 stripping of membranes suggested receptor occupation by exogenous tGH. IGF-I activity, measured by 35SO4 incorporation into oral cartilage explants in vitro, was decreased 50% by hypophysectomy and increased to 200% of intact control levels after injection of 1000 ng tGH/g. In a second experiment, 35SO4 incorporation by oral cartilage from hypophysectomized fish injected with 10, 100 or 1000 ng tGH/g was stimulated to intact control levels. Effects of feeding and tGH injection on in-vitro responsiveness of oral cartilage to recombinant bovine IGF-I (rbIGF-I; 10-1000 ng/ml) were also assessed. Oral cartilage from fed fish showed a parabolic dose-response curve, whereas oral cartilage from starved fish had a lower basal rate of 35SO4 incorporation and a linear dose-response relationship. Oral cartilage from hypophysectomized G. mirabilis showed a significantly attenuated response to rbIGF-I which was restored by tGH injection, suggesting that the GH status of the animal is important for sensitivity of target tissue to IGF-I. Because of its similarity to other vertebrate systems, G. mirabilis presents a good teleost model of growth regulation and of the functions and interactions of GH and IGF-I.

Comparative endocrinology of the insulin-like growth factor-binding protein.

Emerging early in chordate evolution, the IGF-regulatory axis diverged from an insulin-like predecessor into a vertebrate regulatory system specializing in cell growth activation and allied anabolic functions. Essential to the divergence of the IGF and insulin systems was an early presence of soluble IGF-binding proteins (IGFBPs), which bind IGF peptides at much higher affinity than that of the insulin receptor but at comparable affinities to that of the IGF receptor. IGFBPs have no homology with IGF receptors. Instead, IGFBPs are a derived group of proteins within a superfamily of cysteine-rich growth factors, whose members are found throughout the animal taxa. While blocking IGF actions through the insulin receptor is a fundamental role, IGFBPs evolved within the vertebrate line into centralized, 'integrators' of the endocrine growth-regulatory apparatus. IGFBPs have substantial influences on the distribution and bioavailability of IGF peptides in the cellular and physiological environments, but they have a variety of other properties. The six principal mammalian IGFBPs exhibit an array of specialized properties that appear to be derived from a complex evolutionary history (including cell membrane association, interaction with proteins that post-translationally modify them, direct IGF-independent effects on cells, and others) and they are regulated by a diversity of 'outside' factors (e.g. other hormones, metabolic status, stress). Thus, IGFBPs are multifunctional integrators having diverse physiological 'agendas'. Much less is known about IGFBPs and their properties in the other vertebrate taxa. Increasingly, however, it is being recognized that they play equally important endocrine roles, in both conserved and non-conserved ways, when compared with those currently defined in mammals. This review highlights selected 'comparative aspects' in current IGFBP research, in an attempt to view this essential group of endocrine regulators from a wider, biological perspective.

Electrical injury through the eyes of professional electricians.

This paper presents the first results of an attitudinal survey that was conducted among professional electricians in order to explore their knowledge and beliefs related to occupational electrical injury. Four hundred eighty-one out of 1200 questionnaires were returned and analyzed. The presented statistical and qualitative data reflect electricians' personal experiences with electrical injury, their communication patterns around electrical trauma, their understanding of possible electrical injury sequelae, their safety beliefs and attitudes towards occupational dangers, and the reasons for their occupational choice. We expect that the results of this study will enhance our understanding of the psychological profile, environment, and culture of electrical workers. The collected data may also help to identify those at risk for poor outcome after electrical injury and determine a new set of risk factors to be taken into account by medical professionals, social workers, and union/utility training officers.

Management and coordination of postacute medical care for electrical trauma survivors.

The clinical spectrum of electrical injury ranges from the absence of any external physical signs to severe multiple trauma. Reported neuropsychiatric sequelae can vary from vague complaints, which may seem unrelated to the injury in their occurrence over time or by their apparent severity, to sequelae consistent with brain injury accompanying an electrical trauma. In this report, a case study and discussion are presented on the management and coordination of post-acute care of an electrical trauma survivor. Expertise and a multidisciplinary team are essential to cohesive patient care. Patient monitoring for progressive changes and prompt intervention are needed to address the potential difficulties experienced by trauma survivors as they rehabilitate to return to their work and their activities of daily living.

Life after electrical injury. Risk factors for psychiatric sequelae.

Long-term cognitive and emotional deficits have been commonly reported in electrical injury (EI) survivors. However, it remains undetermined what factors may lead to the development of such effects in some patients and not in others. In this study, we hypothesized that certain elements of subjective EI experience may predict specific psychiatric sequelae. A group of 73 post-acute EI patients were included in this retrospective study. Statistical associations were examined between major psychiatric diagnoses (posttraumatic stress disorder and major depression) and such EI descriptors as having experienced "no-let-go" or having been knocked away on contact, as well as loss of consciousness or altered states of consciousness at the scene of the accident (including amnesia for the event). The study results will help physicians determine which patients may be at increased risk of developing psychiatric symptoms and address these issues as part of their total rehabilitation plan.

Effect of epinephrine on net lactate uptake by contracting skeletal muscle.

The purpose of this study was to determine the effect of epinephrine on net lactate (La(-)) uptake at constant elevated blood La(-) concentration and steady level metabolic rate (O(2) uptake) in the canine gastrocnemius-plantaris muscle in situ. Infusion of La(-)/lactic acid (pH 3.5) established a mean arterial blood La(-) concentration of ~10 mM while normal blood-gas and pH status were maintained as the gastrocnemius-plantaris was stimulated with tetanic trains at a rate of one contraction every 4 s. After steady-state control measures, epinephrine was infused for 35 min at rates that produced a high physiological concentration with (Pro; n = 6) and without (Epi; n = 6) beta-adrenergic-receptor blockade via propranolol. Net La(-) uptake values during the control conditions were not significantly different between trials (Epi: 0.756 +/- 0.043; Pro: 0.703 +/- 0.061 mmol. kg(-1). min(-1)). Steady level O(2) uptake averaged approximately 69.5 ml. kg(-1). min(-1) for both control conditions and did not significantly change over the course of the experiments in either set of trials. Epi experiments resulted in a significantly reduced net La(-) uptake (0.346 +/- 0.088 mmol. kg(-1). min(-1) after 5 min of infusion) compared with control value at all sample times measured. However, net La(-) uptake was not significantly different from control at any time during Pro (0.609 +/- 0.052 mmol. kg(-1). min(-1) after 5 min of infusion). When the change from the respective control values for net La(-) uptake was compared across time for both series of experiments, Epi resulted in a significantly greater change from control than did Pro. This study suggests that epinephrine can have a profound effect on net La(-) uptake by contracting muscle and that these effects are elicited through beta-adrenergic-receptor stimulation.

Role of convective O(2) delivery in determining VO(2) on-kinetics in canine muscle contracting at peak VO(2).

A previous study (Grassi B, Gladden LB, Samaja M, Stary CM, and Hogan MC, J Appl Physiol 85: 1394-1403, 1998) showed that convective O(2) delivery to muscle did not limit O(2) uptake (VO(2)) on-kinetics during transitions from rest to contractions at approximately 60% of peak VO(2). The present study aimed to determine whether this finding is also true for transitions involving contractions of higher metabolic intensities. VO(2) on-kinetics were determined in isolated canine gastrocnemius muscles in situ (n = 5) during transitions from rest to 4 min of electrically stimulated isometric tetanic contractions corresponding to the muscle peak VO(2). Two conditions were compared: 1) spontaneous adjustment of muscle blood flow (Q) (Control) and 2) pump-perfused Q, adjusted approximately 15-30 s before contractions at a constant level corresponding to the steady-state value during contractions in Control (Fast O(2) Delivery). In Fast O(2) Delivery, adenosine was infused intra-arterially. Q was measured continuously in the popliteal vein; arterial and popliteal venous O(2) contents were measured at rest and at 5- to 7-s intervals during the transition. Muscle VO(2) was determined as Q times the arteriovenous blood O(2) content difference. The time to reach 63% of the VO(2) difference between resting baseline and steady-state values during contractions was 24.9 +/- 1.6 (SE) s in Control and 18.5 +/- 1.8 s in Fast O(2) Delivery (P < 0.05). Faster VO(2) on-kinetics in Fast O(2) Delivery was associated with an approximately 30% reduction in the calculated O(2) deficit and with less muscle fatigue. During transitions involving contractions at peak VO(2), convective O(2) delivery to muscle, together with an inertia of oxidative metabolism, contributes in determining the VO(2) on-kinetics.

A comparison of in vitro cellular responses to mechanical and electrical stimulation.

In the last several decades, enormous interest has been generated toward understanding the cell as it is controlled by its external physical environment. The purpose of this study was to determine the effects of well-defined applied mechanical stress and time-varying electric fields on the cellular synthesis of connective tissue macromolecules. Chondrocytes harvested by trypsin digestion of 15-day-old chick embryo sternae were randomly dispersed and cultured on elastin membranes in a humidified atmosphere with 10 per cent CO2 and 90 per cent air. Following five days of growth in F12 media and 5 per cent fetal calf serum, the membranes underwent either 1) a 10 per cent cyclic mechanical stretch or 2) 60 Hz A.C. electrical stimulation with current densities of 1 to 1,000 nA/mm2 or 3) control without stimulation, each for an eight-hour period. C14-hydroxyproline incorporation into collagen, and H2 35 SO4 incorporation into glycosaminoglycans (GAGs) were measured by liquid scintillation techniques. Scanning and transmission electron microscopy analysis of control and stimulated cells demonstrated discernable differences. Both mechanically and electrically stimulated chondrocytes showed a two- to three-fold increase in GAG synthesis and a general depression in protein and collagen synthesis over controls. The general similarity in response to both mechanical and electrical stress suggests common processes by which they modulate cellular synthesis of cartilage connective tissue proteins.

Serum insulin-like growth factor binding proteins (IGFBPs) as markers for anabolic/catabolic condition in fishes.

In fishes as well as in all vertebrates in which it has been assessed, physiological shifts toward catabolism (e.g. such as during food deprivation) are consistently associated with elevations in the serum levels of at least one (often two in fishes) IGFBP in the < or =31-kDa size range. In mammals, 30-kDa IGFBP-1 is strongly up-regulated under catabolic circumstances, and it plays an important physiological role by sequestering IGF peptides to inhibit energy-expensive growth until conditions are more favorable (e.g. with resumed feeding). Similarly in fishes, it has been found that when the < or =31-kDa IGFBPs are elevated in serum, somatic growth is inhibited, suggesting a similar growth-inhibitory role of these proteins to that of mammalian IGFBP-1. Three different experimentally-induced catabolic states in fishes are compared in this paper: fasting; insulin-dependent diabetes mellitus (IDDM); and stress. A strong relationship between elevated serum cortisol concentrations and the presence of IGFBPs in each case is noted, and the utility of serum IGFBP measurement to serve as an effective indicator (marker) of catabolic condition in fishes is discussed.