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PubMed1989

[Inhibition of pancreatic beta-cell secretion during a "glucose-clamp" in subjects with acanthosis nigricans].

It has long been known that acanthosis nigricans is accompanied by insulin resistance. In certain insulin-resistant states, including obesity, a more sluggish response to the insulin/insulin inhibition feedback normally present in pancreatic beta cells has been documented. Some have claimed a sort of beta-cell insulin resistance "parallel" to that of the peripheral tissues. The present study assesses the efficiency of the insulin/insulin feedback in acanthosis nigricans patients, measuring the inhibition of the production of C-peptide (the indicator of beta cell secretion) induced by the administration of exogenous insulin during glucose clamping. This was done in order to compare the roles of the peripheral tissues and the beta cells in producing the insulin resistance typical of acanthosis nigricans. The study using the glucose-insulin clamp technique was conducted on 4 Acanthosis Nigricans patients with normal glucose tolerance and 4 healthy controls, the drop in C-peptide levels after the administration of exogenous insulin being assessed in the course of both steady states. The results showed that the acanthosis nigricans patients retained a beta cell response to the exogenous insulin through their peripheral tissues presented a reduced sensitivity to insulin as revealed by the glucose-insulin clamp. It therefore seems reasonable to attribute the endocrine metabolic alteration found in Acanthosis Nigricans to a peripheral receptor and/or post receptor alteration rather than central alterations in the beta cells that have yet to be demonstrated. It is concluded that in acanthosis nigricans the peripheral insulin resistance is primarily independent phenomenon and not "parallel" to insulin/insulin feedback.

Acanthosis Nigricans↗
PubMed2001

Expression and localization of endothelin receptors: implications for the involvement of peripheral glia in nociception.

The endothelins (ETs) are peptides that have a diverse array of functions mediated by two receptor subtypes, the endothelin A receptor (ET(A)R) and the endothelin B receptor (ET(B)R). Pharmacological studies have suggested that in peripheral tissues, ET(A)R expression may play a role in signaling acute or neuropathic pain, whereas ET(B)R expression may be involved in the transmission of chronic inflammatory pain. To begin to define the mechanisms by which ET can drive nociceptive signaling, autoradiography and immunohistochemistry were used to examine the distribution of ET(A)R and ET(B)R in dorsal root ganglia (DRG) and peripheral nerve of the rat, rabbit, and monkey. In DRG and peripheral nerve, ET(A)R-immunoreactivity was present in a subset of small-sized peptidergic and nonpeptidergic sensory neurons and their axons and to a lesser extent in a subset of medium-sized sensory neurons. However, ET(B)R-immunoreactivity was not seen in DRG neurons or axons but rather in DRG satellite cells and nonmyelinating ensheathing Schwann cells. Thus, when ETs are released in peripheral tissues, they could act directly on ET(A)R-expressing sensory neurons and on ET(B)R-expressing DRG satellite cells or nonmyelinating Schwann cells. These data indicate that ETs can have direct, nociceptive effects on the peripheral sensory nervous system and that peripheral glia may be directly involved in signaling nociceptive events in peripheral tissues.

Animals↗
PubMed1983

Tissue glucose and lactate metabolism and interconversions in pregnant and lactating sheep.

Continuous infusions of [14C]glucose and [14C]lactate on separate days, and measurements of blood flow-rate, were used to obtain values for rates of unidirectional metabolism and of interconversion of glucose and lactate in the portal-drained viscera, liver and hind-quarters of ewes during late pregnancy and early lactation. All infusions were made within 5 h after the morning meal, when steady-state conditions appeared to exist. Use was made of ewes that had been appropriately catheterized during pregnancy, and whose catheters remained patent through into lactation. The liver was the main source of glucose production (67-70%) during both pregnancy and lactation. Other sources were the portal-drained viscera (absorbed glucose) and, presumably, the kidneys. Over 80% of the glucose was utilized by the peripheral tissues with approximately 35-40% of utilization being attributable to the hind-quarters. Of the total lactate production, 76% occurred in the peripheral tissues during pregnancy but only 36% during lactation. While the liver utilized 73% of lactate during pregnancy, this value fell to only 42% during lactation, at which time the portal-drained viscera utilized 26% of the lactate. During pregnancy, approximately 80% of the lactate arose from glucose, chiefly in peripheral tissues, while at least 12% of the glucose arose from lactate, chiefly in the liver. During lactation the extent of these interconversions was decreased. Despite the interconversions, whole-body turnover rates for glucose and lactate were under- or overestimated by only 4-10% and 2-5% respectively. Furthermore, a comparison of turnover rates obtained with [U-14C]- and [6-3H]glucose indicated that there was only 6 and 2% recycling of glucose-C during pregnancy and lactation respectively. Under the conditions employed in this study, lactate does not appear to be a major precursor of glucose in the ruminant, and most of the lactate taken up by the liver must be used for purposes other than gluconeogenesis, such as oxidation or alternative anabolic pathways.

Animals↗
PubMed2004

Expression of membrane and nuclear melatonin receptors in mouse peripheral organs.

Previous studies have shown that melatonin acts through specific receptors, including MT(1) and MT(2) membrane receptors as well as a nuclear receptor belonging to the orphan nuclear receptor family. Therefore, the goal of this study was to determine whether melatonin receptors mRNA is expressed in mouse peripheral tissues. To study the different receptors subtype expression, we have used a reverse-transcription polymerase chain reaction (RT-PCR) procedure followed by Southern hybridization with specific digoxigenin-labeled probes. RT-PCR studies revealed the presence of both MT(1) membrane receptors and ROR(alpha)1 nuclear receptors in all the peripheral tissues examined (brain, heart, lung, liver and kidney). Moreover, the expression of ROR(alpha)1 nuclear receptors was also demonstrated by Western-blot. In contrast, expression of MT(2) membrane receptors was only observed in brain and lung. These results suggest that melatonin, acting through its different subtypes receptors, plays a role in the neuroendocrine regulation of peripheral tissues function.

Animals↗
PubMed1995

The 3' flanking region of the human tyrosine hydroxylase gene directs reporter gene expression in peripheral neuroendocrine tissues.

Cell type-specific expression of the catecholamine synthetic enzyme, tyrosine hydroxylase (TH), appears to be mediated in part by cis-acting elements located at the 3' end of the human gene. Further delineation of this region indicated sequences corresponding to a CACGTG motif significantly stimulated transcription of a heterologous promoter in various cell types. Mutation of this site led to a complete loss of activity. DNase footprinting, gel retardation, and UV cross-linking experiments indicated that a 74-kDa cellular factor(s) bound specifically to the CACGTG motif in the pheochromocytoma cell line PC12. The size of this protein and its pattern of expression are compatible with those of the CACGTG binding protein TFE3. Transgenic animals were created using a 261-bp human TH 3' fragment encompassing the CACGTG motif in front of a thymidine kinase promoter/chloramphenicol acetyltransferase reporter gene. In three lines of mice this fragment was sufficient to direct a pattern of mRNA expression in peripheral neuroendocrine tissues that mimicked TH mRNA distribution. However, these sequences were not sufficient for CNS-specific patterns of expression. Thus, multiple cell type-specific enhancers may regulate TH gene expression in the CNS and periphery.

Animals↗
PubMed2006

Regulation of metal transporters by dietary iron, and the relationship between body iron levels and cadmium uptake.

Iron (Fe) plays essential roles in biological processes, whereas cadmium (Cd) is a toxic and non-essential metal. Two metal transporters, divalent metal transporter 1 (DMT1) and metal transporter protein 1 (MTP1), are responsible for Fe transport in mammals. Here, we studied the effect of dietary Fe on the expression of these metal transporters in peripheral tissues, and the uptake by these tissues of Cd. Mice were fed an Fe-sufficient (FeS: 120 mg Fe/kg) or Fe-deficient (FeD: 2-6 mg Fe/kg) diet for 4 weeks. The total Fe levels in the body were evaluated by measuring tissue Fe concentrations. Tissue Cd concentrations were determined 24 h after the mice received a single oral dose of Cd. Animals fed a FeD diet showed depletion of body Fe levels and accumulated 2.8-fold higher levels of Cd than the FeS group. Quantitative real time RT-PCR revealed that whereas DMT1 and MTP1 were both ubiquitously expressed in all FeS peripheral tissues studied, DMT1 was highly expressed in brain, kidney, and testis, whereas MTP1 was highly expressed in liver and spleen. Depletion of the body Fe stores dramatically upregulated DMT1 and MTP1 mRNA expression in the duodenum as well as moderately upregulating their expression in several other peripheral tissues. The iron response element positive isoform of DMT1 was the most prominently upregulated isoform in the duodenum. Thus, DMT1 and MTP1 may play an important role in not only maintaining Fe levels but also facilitating the accumulation of Cd in the body of mammals.

Animals↗
PubMed1988

Phenotypic analysis of synovial tissue and peripheral blood lymphocytes isolated from patients with rheumatoid arthritis.

Cytofluorometric analysis was performed to characterize the surface phenotype and activation status of freshly isolated synovial tissue lymphocytes (STL) and peripheral blood lymphocytes (PBL) from 7 patients with rheumatoid arthritis (RA). Proliferative synovium was enzymatically digested to obtain tissue-derived lymphocytes. Indirect immunofluorescent staining of patient PBL and STL with a variety of monoclonal antibodies failed to reveal a consistent alteration in the number of CD4+ (helper/inducer) PBL or STL. However, there was a significant decrease in the number of CD8+ (suppressor/cytotoxic) cells in rheumatoid STL (P less than 0.05). A significant reduction in the density of the T cell differentiation antigens CD3 and CD4 was observed in RA PBL and STL, compared with control PBL. These differences in antigen density were not seen when normal PBL were subjected to the same enzymatic digestion. Both RA PBL and STL manifested increased expression of HLA-DR antigens, without augmentation of interleukin-2 receptor expression. Alterations in the expression of the T cell differentiation antigens and activation antigens by patient PBL closely paralleled the abnormalities observed in STL. In contrast, STL of patients with RA exhibited an increase in the expression of the adhesion-related glycoproteins (leukocyte function-associated 1 [LFA-1] and very late activation 1 [VLA-1] antigens), not observed with autologous PBL. These studies demonstrate that lymphocytes isolated from the synovial tissues of RA patients bear an activated phenotype, exemplified by the modulation of CD3 and CD4 and the expression of HLA-DR.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens↗
PubMed2003

Optimization of Schwann cell adhesion in response to shear stress in an in vitro model for peripheral nerve tissue engineering.

The design of nerve guidance channels (NGCs) is evolving to produce a favorable environment for neural regeneration. We created an in vitro model to evaluate the interactions between three centrally important components of this altered host environment: (1). Schwann cells, (2). substrate, and (3). sustained mechanical stimulus in the form of shear stress with laminar fluid flow. Preconfluent Schwann cells were plated on slides coated either with laminin, poly-D-lysine, type IV collagen, or fibronectin. These slides were placed into custom-designed, parallel-plate, flow chambers and were administered laminar fluid flow at a rate of 15 mL/min for 2 h. Schwann cell adhesion assays demonstrated that laminin (mean, 86.1%; SEM, 4.47%) and fibronectin (mean, 81.7%; SEM, 3.24%) were statistically superior to collagen type IV (mean, 57.7%; SEM, 3.96%) and poly-D-lysine (mean, 58.0%; SEM, 4.97%) (p < 0.001). Fibronectin (mean, 12.20%; SEM, 0.374%) induced statistically greater Schwann cell proliferation than did laminin (mean, 8.14%; SEM, 0.682%) (p < 0.001). Therefore, we recommend that fibronectin should be used as an important component of NGCs with further in vivo studies. As mechanical stress is an integral part of the host environment, our study is the first to incorporate this factor into an in vitro model for peripheral nerve tissue engineering.

Animals↗
PubMed1997

Peripheral noradrenergic turnover in streptozotocin-induced diabetic rats.

Our goal was to determine whether basal sympathetic tone to the kidney and various peripheral tissues is altered in conscious diabetic rats. Norepinephrine (NE) turnover was determined by measuring the decline in tissue NE concentration ([NE]) at 4 and 8 h after administering alpha-methyl-p-tyrosine to animals from each of three groups, diabetic (STZ injected 4 weeks prior to experimentation), diabetic + insulin (STZ injected; insulin injected; 2 U/day per rat for 4 weeks) and control (n = 18-20 per group). Various peripheral tissues (duodenum, left ventricle of the heart, kidney, skeletal muscle, left adrenal gland and liver) were examined. [NE] was significantly increased in the kidney and liver, but decreased in the duodenum of the diabetic compared to the control rats. In contrast to the changes in [NE], the rate constant, which provides an index of sympathetic tone, increased in the duodenum and liver, and a decreased in the adrenal gland. The turnover of NE, which is a composite of [NE] and rate constant, increased in the kidney and liver, and decreased in the adrenal gland of diabetic rats. Chronic treatment of diabetic rats with insulin normalized NE turnover in the liver, but not in the adrenal gland. Diabetic rats treated with insulin exhibited a reduced turnover of NE in the kidneys. These data demonstrate that there are differential changes in the [NE], rate constant, and turnover of NE in diabetic rats. Overall, these data indicate that there is increased noradrenergic activity to the kidney, possibly related to sodium retention, and a differential change in noradrenergic activation to various peripheral tissues in diabetic rats.

Animals↗
PubMed1988

Local generation and release of angiotensin II in peripheral vascular tissue.

Isolated rat hindlegs were perfused with Krebs-Ringer solution, and immunoreactive angiotensin II (irAng II) released into the perfusate was directly determined using a Sep-Pak C18 cartridge connected to the perfusion system. High performance liquid chromatography clearly demonstrated the presence of angiotensin I (Ang I), angiotensin II (Ang II), and a small amount of angiotensin III. The spontaneous release of irAng II was as high as about 600 pg/30 min, which was stable up to 3 hours. Captopril added to the perfusion medium (10(-9) to 10(-6) M) suppressed irAng II release in a dose-dependent manner (p less than 0.001), and it (10(-6)M) caused a reciprocal increase of irAng I release (p less than 0.05). Oral pretreatment of captopril (50 mg/kg/day) for 1 week suppressed the irAng II release by 31% (p less than 0.02). The same treatment with SA 446, a highly lipophilic angiotensin converting enzyme inhibitor, inhibited the irAng II release by 63% (p less than 0.001). On the other hand, the two inhibitors suppressed the plasma irAng II to very similar extents. Pretreatment with SA 446 plus nephrectomy did not cause any further change in irAng II release as compared with that with SA 446 alone. These results provide direct proof for local generation and subsequent secretion of Ang II by peripheral vascular tissue.

3-Mercaptopropionic Acid↗
PubMed2005

Novel stressors affected catecholamine stores in socially isolated normotensive and spontaneously hypertensive rats.

Catecholamines in some central (hypothalamus and hippocampus) and peripheral tissues (adrenal glands and heart auricles) of long-term socially isolated normotensive and spontaneously hypertensive rats exposed to novel immobilization stress were determined by a simultaneous single isotope radioenzymatic assay. Long-term isolation (21 days) produced depletion of hypothalamic norepinephrine (NE) stores and hippocampal dopamine (DA) stores in both normotensive and spontaneously hypertensive rats. Acute immobilization stress (2 h) significantly decreased NE and DA stores in hypothalamus and hippocampus of naive normotensive and spontaneously hypertensive rats controls. However, novel immobilization stress applied to normotensive rats previously subjected to long-term isolation produced no changes in catecholamine levels in hypothalamus, while resulting in somewhat higher depletion of NE stores in hypothalamus of spontaneously hypertensive rats treated in the same way. Novel immobilization stress decreased NE and DA stores in hippocampus of normotensive but was without effect on NE and DA stores of spontaneously hypertensive rats. Social isolation did not affect catecholamine stores in peripheral tissues but novel immobilization stress produced a significant decrease in catecholamine content. The results suggest that some central and peripherals tissues of spontaneously hypertensive rats and normotensive rats differ with regard to catecholamine content and that there are certain differences in their responsiveness to stress.

Adrenal Glands↗
PubMed1980

Effects of pregnancy and lactation on the peripheral lymphatic tissue in the mouse: qualitative and quantitative morphology.

Effects of pregnancy and lactation on the spleen and the mesenteric, iliac, axillary and popliteal lymph nodes in the mouse were morphologically examined by means of qualitative and quantitative methods. During pregnancy the spleen weight increases to reach a peak at 15 days of pregnancy. After parturition the weight decreases gradually until 20 days postpartum when it has returned to almost normal. Both the red and white pulps increase in volume during pregnancy. After parturition, the volume of the white pulp rapidly returns to normal. The volume of the red pulp remains greater in lactating females than in control females. In non-lactating females the red pulp decreases rapidly in volume after parturition. In the spleen, plasma cells increase in number during pregnancy, and often contain Russell bodies. They are accumulated in large numbers particularly in the marginal zone and periarterial area. After parturition plasma cells decrease rapidly in number. The weight of the mesenteric lymph node undergoes a slight but a significant increase during pregnancy, and decreases in both the lactating and non-lactating groups after parturition. During pregnancy the medulla shows an increase in volume, and the medullary cords are filled with numerous plasma cells. At 10--15 days of pregnancy, plasma cells also occur in groups in the paracortex. They decrease rapidly after parturition. During pregnancy plasma cells are also markedly increased in iliac lymph nodes, but not in axillary and popliteal lymph nodes. The findings were discussed particularly in relation to the immune response of the peripheral lymphatic tissue in pregnancy.

Animals↗
PubMed2003

Ryegrass-based diet and barley supplementation: partition of nitrogenous nutrients among splanchnic tissues and hind limb in finishing lambs.

Splanchnic metabolism of nitrogenous nutrients and their uptake by the hind limb were studied in finishing lambs receiving ryegrass harvested at grazing stage with or without barley supplementation. Six multicatheterized lambs (40.2 +/- 1.5 kg) were fed with frozen ryegrass (RG) at 690 kJ of ME intake (MEI) x d(-1) x BW(-0.75) and 20.8 g of N intake (NI)/d successively without and with barley supplementation (RG + B), according to a crossover design. Barley supplementation represented 21% of DM intake and increased the MEI and the NI by 32 and 24% respectively, (P < 0.01). In the ruminal fluid, barley increased acetate and butyrate concentrations by 21.2 and 49.6%, respectively (P < 0.04), without any effect on the ammonia concentration. Consequently, the net portal appearance (NPA) of ammonia was not modified, but the NPA of total amino acids (TAA; +38%) and nonessential amino acids (NEAA; +45%) was increased (P < 0.05) by barley supplementation. Taken individually, the NPA of the essential amino acids (EAA) was increased for isoleucine (+32%; P < 0.05), threonine (+151%; P < 0.03), and lysine (+26%; P < 0.06), with no effect for the other EAA. In contrast to what was observed at the PDV level, no significant alteration in the net hepatic amino acid flux was observed for TAA, EAA, NEAA, branched-chain amino acids (BCAA), urea, and ammonia after barley supplementation, showing a relatively minor role of the liver in the regulation of the supply of amino acids to the peripheral tissues. However, taken individually, the net hepatic uptake of some NEAA involved in gluconeogenesis and/or ureagenesis was altered with barley supplementation: the alanine uptake was increased by 44% (P < 0.05), aspartate + asparagine (asx) uptake was decreased by 18% (P < 0.01), and glutamate + glutamine (glx) release tended (P < 0.10) to be increased by 208%. With barley supplementation, NI increased by 5 g of N/d, and net splanchnic release increased by 4.63 g of N/d. Consequently, the additional dietary N supply (together with energy supply) was nearly exclusively available to peripheral tissues as AA-N (N as amino acids), but no strong effect of this additional supply of AA to the hind limb could be demonstrated in terms of net AA hind limb fluxes. Consequently, barley supplementation of a ryegrass-based diet increased the net AA release by the splanchnic tissues, with little effect on the AA net uptake by the peripheral tissues.

Amino Acids, Essential↗
PubMed1993

Demonstration of large-scale migration of cortical thymocytes to peripheral lymphoid tissues in cyclosporin A-treated rats.

Young adult Lewis rats were maintained on diets containing 0.015 or 0.027% cyclosporin A (CSA) for periods of up to 6 wk. All animals showed complete depletion of medullary thymocytes (CD4+8- and CD4-8+, T cell receptor [TCR] alpha/beta hi, Thy-1med/low, terminal deoxynucleotidyl transferase negative [TdT-]) and a 50% reduction in the number of TdT- cortical thymocytes (CD4+8+, TCR alpha/beta low, Thy-1med) within 1 wk of CSA treatment. In addition, about half of the animals displayed a 50% reduction in the number of TdT+ cortical thymocytes (CD4+8+, TCR alpha/beta low, Thy-1hi). These intrathymic changes were accompanied by a reciprocal increase in the number of double-positive (DP; CD4+8+) T cells in lymph nodes (LN) and spleens. To confirm that the latter T cells were recent thymic emigrants (RTE), CSA-treated rats were injected intrathymically with fluorescein isothiocyanate, and the phenotype of the labeled T cells appearing in LN was determined 16 h later. The results demonstrated that, in addition to those RTE exported in normal animals (> 90% medullary origin), the emigration of DP thymocytes, including large numbers of TdT+ thymocytes, was markedly increased. The presence of TdT+ cells, which normally do not leave the thymus, clearly identifies the DP RTE as originating from the thymus cortex. Intrathymic labeling studies also directly demonstrated that export of all thymocyte subsets ceases within 9 d of CSA treatment; and thymectomy experiments confirmed that the CSA-induced increase in phenotypically immature T cells resulted primarily from the disturbance of thymocyte maturation and emigration, rather than from a direct effect on preexisting T cells. These results suggest that a wave of cortical thymocytes, many of which presumably have not yet undergone negative selection, is released from the thymus during the first week of CSA treatment. The presence of these potentially unselected cells in peripheral lymphoid tissues may help to explain the increased frequency of autoreactive T cells observed in CSA-treated animals.

Animals↗
PubMed2000

Vanadate restores glucose 6-phosphate in diabetic rats: a mechanism to enhance glucose metabolism.

Vanadate mimics the metabolic actions of insulin. In diabetic rodents, vanadate also sensitizes peripheral tissues to insulin. We have analyzed whether this latter effect is brought about by a mechanism other than the known insulinomimetic actions of vanadium in vitro. We report that the levels of glucose 6-phosphate (G-6-P) in adipose, liver, and muscle of streptozotocin-treated (STZ)-hyperglycemic rats are 77, 50, and 58% of those in healthy control rats, respectively. Normoglycemia was induced by vanadium or insulin therapy or by phlorizin. Vanadate fully restored G-6-P in all three insulin-responsive peripheral tissues. Insulin did not restore G-6-P in muscle, and phlorizin was ineffective in adipose and muscle. Incubation of diabetic adipose explants with glucose and vanadate in vitro increased lipogenic capacity three- to fourfold (half-maximally effective dose = 11 +/- 1 microM vanadate). Lipogenic capacity was elevated when a threshold level of approximately 7.5 +/- 0.3 nmol G-6-P/g tissue was reached. In summary, 1) chronic hyperglycemia largely reduces intracellular G-6-P in all three insulin-responsive tissues; 2) vanadate therapy restores this deficiency, but insulin therapy does not restore G-6-P in muscle tissue; 3) induction of normoglycemia per se (i.e., by phlorizin) restores G-6-P in liver only; and 4) glucose and vanadate together elevate G-6-P in adipose explants in vitro and significantly restore lipogenic capacity above the threshold of G-6-P level. We propose that hyperglycemia-associated decrease in peripheral G-6-P is a major factor responsible for peripheral resistance to insulin. The mechanism by which vanadate increases peripheral tissue capacity to metabolize glucose and to respond to the hormone involves elevation of this hexose phosphate metabolite and the cellular consequences of this elevated level of G-6-P.

Adipose Tissue↗
PubMed2006

Structure and expressions of two circadian clock genes, period and timeless in the commercial silkmoth, Bombyx mori.

We cloned two circadian clock genes period (Bmper) and timeless (Bmtim) from the commercial silkmoth, Bombyx mori. Sequence analysis revealed a high degree of conservation among insects for both genes. BmPER predicted from the DNA sequence is a polypeptide of 1, 113 amino acids with functional domains such as PAS, PAC, nuclear localization signal (NLS) and cytoplasmic localization domain (CLD). Deduced BmTIM consists of 997 amino acids with PER interaction site (PIS) as well as NLS and CLD. Southern blot analyses revealed that Bmper and Bmtim are single copy genes. Northern blot analysis demonstrated that Bmper and Bmtim are expressed both in the head and peripheral tissues. We also examined temporal profiles of Bmper and Bmtim expressions in the head, flight muscle, testis and antenna of adult males under LD12:12 and LD16:8 by Real-Time PCR assays. Our data show that photoperiod differentially affects the temporal expression patterns of Bmper and Bmtim. The mRNA expression of Bmper and Bmtim in the head had a phase lead under LD12:12 compared to that under LD16:8, whereas photoperiod did not affect expression patterns in peripheral tissues relative to light-on. Photoperiod affected not only the phase relationship but also the expression level. In the testis and antenna, the level of transcription of Bmtim was low in LD12:12 but high in LD16:8. The daily differences in amplitudes of the Bmper and Bmtim expression rhythms were 2-fold in the head and 1.5-2.5 folds in the peripheral tissues examined.

Amino Acid Sequence↗
PubMed1997

Phenotypic variability of CADASIL and novel morphologic findings.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a non-arterio-atherosclerotic, non-amyloidotic arteriopathy affecting preferentially the small arteries and arterioles of the brain. The morphologic hallmark is the presence of a characteristic granular alteration of the arterial media that ultrastructurally corresponds to the accumulation of electron-dense material surrounding the smooth muscle cells. Although the presence of this granular osmiophilic material (GOM) was originally described as limited to brain vessels, identical electron microscopic findings have been demonstrated in the media of peripheral tissue arteries, allowing for a pathologic diagnosis of the disease by a simple skin, muscle or nerve biopsy. We report some atypical features identified in our CADASIL patients that broaden the phenotypic expression of this disease. Firstly, we identified a cortical infarct in an otherwise typical CADASIL patient. Secondly, we observed GOM in skin arteries of a 30-year-old man with hemiplegic migraine, the son of a woman who had died with CADASIL. This confirms that it may be possible to diagnose the disease at a preclinical stage by the ultrastructural evaluation of peripheral tissue biopsy material, particularly for individuals for whom there is a supporting family history. Thirdly, ultrastructural examination of the skin, and subcutaneous and striated muscle of an unrelated and apparently sporadic patient with neuropathologic and neuroradiologic evidence of CADASIL in meningeal and cerebral vessels failed to reveal diagnostic lesions in peripheral arteries. Thus, the possibility of a false-negative pathologic diagnosis in patients with a clinicoradiologic diagnosis of CADASIL, if one relies solely on a peripheral tissue biopsy, does exist. Additionally, we have identified heat shock proteins (Hsp70 and alphaB crystallin) and ubiquitin in the vascular myocytes of affected arteries. B crystallin also seemed to be deposited extracellularly, which suggests that GOM also might be immunoreactive for alphaB crystallin.

Adult↗
PubMed1984

In vivo labelling in several rat tissues of 'peripheral type' benzodiazepine binding sites.

'Peripheral type' benzodiazepine binding sites in several rat tissues were labelled by intravenous injection of [3H]PK 11195 and [3H] RO5 -4864. Binding was saturable in all tissues studied and regional distribution paralleled the in vitro binding. A similar potency order of displacing compounds was found in vivo and in vitro PK 11195 greater than PK 11211 greater than RO5 -4864 greater than diazepam greater than dipyridamole greater than clonazepam. These results demonstrate the feasibility of using this technique to examine the effects of pharmacological manipulation on the binding sites in their native state. However some properties (broader maximum during time course, higher percentage of particulate binding in the brain and independence of temperature) make [3H]PK 11195 the most suitable ligand for this kind of studies.

Animals↗