[Advances in application of functional magnetic resonance imaging in patients with painful temporomandibular disorders].

Temporomandibular disorders (TMD), characterized by pain and dysfunction of the temporomandibular joint, are the most common chronic orofacial pain. However, the etiologies and pathologies of TMD related chronic pain are poorly understood. Functional magnetic resonance imaging (fMRI) measures brain activity by detecting changes associated with blood flow without invasiveness, and has been widely used in chronic pain research. We reviewed recent fMRI studies exploring the brain changes of patients with painful TMD to investigate the role of central nervous system in abnormal pain perception and impaired pain modulation, and to summarize the effects of splint therapy, in the hope of facilitating the clinical diagnosis and treatment of TMD.

First Report of a Group 16SrI Phytoplasma Associated with Amaranthus hypochondriacus Cladodes in China.

Amaranthus spp. are cultivated worldwide as leafy vegetable, cereal, and ornamentals. In China, stems and leaves of Amaranthus hypochondriacus L. are used as a vegetable (2). In July 2010, sporadic amaranth plants exhibiting symptoms of cladodes and spica proliferation were observed in a vegetable garden near Foshan, Guangdong, China. Stem samples were collected from two symptomatic and two asymptomatic plants. Total DNA was extracted with a modified cetyltrimethylammonium bromide (CTAB) method (1). Nested PCR with a combination of phytoplasma-specific universal primer pairs (P1/P7 and R16F2n/R16R2) amplified 16S rDNA sequences with the expected size of 1.2 kb from all samples of symptomatic amaranth plants, but not from the asymptomatic plants (3). Nested PCR products yielded identical AluI, HhaI, HpaII, HaeIII, KpnI, MseI, RsaI, Sau3AI, and TaqI restriction fragment length polymorphism (RFLP) profiles with chinaberry witches'-broom phytoplasma (16SrI-B subgroup), but different from peanut witches'-broom phytoplasma (16SrII group), jujube witches'-broom phytoplasma (16SrV group), and paulownia witches'-broom phytoplasma (16SrI-D subgroup). Nested PCR products were purified, cloned in pMD18-T Simple Vector (TaKaRa, Dalian, China), and sequenced. The 16S rDNA sequences were identical and deposited in GenBank (Accession No. JF323034). GenBank BLASTn analysis indicated that the amaranth extracts showed as high as 99% sequence identity with the members of 16SrI group phytoplasmas, including those associated with arecanut yellow leaf disease (FJ998269) and aster yellow AY-27 (HM467127). A polygenetic tree was constructed using MEGA 4.0 based on the 16S rDNA sequences of amaranth cladode phytoplasma and other phytoplasmas belonging to 16SrI phytoplasma group. In phylogenetic analysis, the sequences clustered on a single branch with members of 16SrI-B subgroup in the tree. Therefore, the phytoplasma was classified in subgroup 16SrI-B. To our knowledge, this is the first report of a subgroup 16SrI-B phytoplasma associated with diseased A. hypochondriacus in China. References: (1) E. Angelini et al. Vitis 40:79, 2001. (2) M. Costea et al. Econ. Bot. 57:646, 2003. (3) I. M. Lee et al. Int. J. Syst. Bacteriol. 48:1153, 1998.

Interleukin-1beta release in the supraoptic nucleus area during osmotic stimulation requires neural function.

Interleukin (IL)-1beta is present throughout the magnocellular neuroendocrine system and co-depletes with oxytocin and vasopressin from the neural lobe during salt-loading. To examine whether IL-1beta is released from the dendrites/soma of magnocellular neurones during osmotic stimulation, microdialysis adjacent to the supraoptic nucleus (SON) in conscious rats was combined with immunocapillary electrophoresis and laser-induced fluorescence detection to quantify cytokine in 5-min dialysates collected before (0-180 min; basal), and after (180-240 min), hypertonic saline injected s.c. (1.5 m NaCl). Osmotic release of IL-1beta was compared after inhibiting local voltage-gated channels for Na+ (tetrodotoxin) and Ca2+ (cadmium and nickel) or by reducing intracellular Ca2+ stores (thapsigargin). Immunohistochemistry combined with microdialysis was used to localise cytokine sources (IL-1beta+) and microglia (OX-42+). Under conditions of microdialysis, the basal release of IL-1beta+ in the SON area was measurable and stable (pg/ml; mean +/- SEM) from 0-60 min (2.2 +/- 0.06), 60-120 min (2.32 +/- 0.05) and 120-180 min (2.33 +/- 0.06), likely originating locally from activated microglia (OX42+; IL-1beta+; ameboid, hypertrophied) and magnocellular neurones expressing IL-1beta. In response to osmotic stimulation, IL-1beta increased progressively in dialysates of the SON area by a mechanism dependent on intracellular Ca2+ stores sensitive to thapsigargin and, similar to dendritic secretion of oxytocin and vasopressin, required local voltage-gated Na+ and Ca2+ channels for activation by osmoregulatory pathways from the forebrain. During osmotic stimulation, neurally dependent release of IL-1beta in the SON area likely upregulates osmosensitive cation currents on magnocellular neurones (observed in vitro by others), to facilitate dendritic release of neurohypophysial hormones.

Response of interleukin-1beta in the magnocellular system to salt-loading.

Drinking 2% NaCl decreases interleukin (IL)-1beta in the neural lobe and enhances IL-1 Type 1 receptor expression in magnocellular neurones and pituicytes. To quantify cytokine depletion from the neural lobe during progressive salt loading and determine whether the changes are reversible and correspond with stores of vasopressin (VP) or oxytocin (OT), rats were given water on day 0 and then 2% NaCl to drink for 2, 5, 8 or 5 days followed by 5 days of water (rehydration). Control rats drinking only water were pair-fed amounts eaten by 5-day salt-loaded animals. Animals were decapitated on day 8, the neural lobe frozen and plasma hormones analysed by radioimmunoassay (OT, VP) or enzyme-linked immunosorbent assay (IL-1beta). IL-1beta, VP and OT in homogenates of the neural lobe were quantified by immunocapillary electrophoresis with laser-induced fluorescence detection. Differences were determined by ANOVA, Tukey's t-test, Dunnett's procedure, Fisher's least significant difference and linear regression analysis. In response to salt-loading, rats lost body weight similar to pair-fed controls, drank progressively more 2% NaCl and excreted greater urine volumes. Plasma VP increased at days 2 and 8 of salt-loading, whereas osmolality, OT and cytokine were enhanced after 8 days with IL-1beta remaining elevated after rehydration. In the neural lobe, all three peptides decreased progressively with increasing duration of salt-loading (IL-1beta, r2 = 0.98; OT, r2 = 0.94; VP, r2 = 0.93), beginning on day 2 (IL-1beta; VP) or 5 (OT), with only VP replenished by rehydration. IL-1beta declined more closely (P < 0.0001; ANOVA interaction analysis) with OT (r2 = 0.96) than VP (r2 = 0.86), indicative of corelease from the neural lobe during chronic dehydration. Local effects of IL-1beta on magnocellular terminals, pituicytes and microglia in the neural lobe with activation of forebrain osmoregulatory structures by circulating cytokine may sustain neurosecretion of OT and VP during prolonged salt-loading.

NO inhibition of the magnocellular neuroendocrine system in rats is independent of cGMP signaling pathway.

Our objective was to test the hypothesis that the cGMP signal-transduction mechanism mediates nitric oxide's (NO) modulation of oxytocin (OT) and vasopressin (VP) secretion from the hypothalamo-neurohypophysial system. Three studies were conducted in adult male Sprague-Dawley rats: (1a) Euhydrated rats received an intracerebroventricular (icv) infusion (1 microl/min for 30 min) of artificial cerebrospinal fluid (aCSF), vehicle (2.6% dimethyl sulfoxide [DMSO]) or 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) (0.05 microg/microl), an inhibitor of soluble guanylyl cyclase (sGC). ODQ did not affect basal levels of plasma VP or OT; (1b) Rats dehydrated for 24 h received aCSF or 8-Br-cGMP (icv), a membrane-permeable analog of cGMP, and plasma hormones were measured 2 min later. 8-Br-cGMP did not significantly change VP or OT levels; (2) Rats ingested water or 2% NaCl for 4 days, and NO synthase (NOS) and sGC activities were measured in posterior pituitaries, the anatomical site of hormone secretion. Salt loading enhanced (P < 0.001) production of [(14)C]citrulline, the coproduct of NO synthesis, without altering cGMP; (3) One SON was microdialyzed with [(14)C]arginine and NOS and sGC activities were quantified in microdialysates during intravenous (iv) infusion of isotonic or hypertonic saline in awake and anesthetized rats. In awake rats, [(14)C]citrulline recovery, but not cGMP, increased (P < 0.05) during intravenous infusion of both isotonic and hypertonic solutions, and after insertion of microdialysis probe itself. In anesthetized rats, however, where basal NOS activity is low, intravenous infusion of hypertonic, but not isotonic solution, increased [(14)C]citrulline recovery without affecting cGMP. Thus, in the forebrain, neither NO produced basally nor during osmotic stimulation depends on cGMP to modulate plasma vasopressin and oxytocin secretion.

Central interactions between angiotensin II and PGD(2) in the regulation of vasopressin and oxytocin secretion in dehydrated rats.

Brain-derived angiotensin II (ANG II) and prostaglandins have important roles in the regulation of body fluid and blood pressure homeostasis. In the present studies we investigated the central interactions between these two neurochemical products in regulating the hypothalamo-neurohypophysial system during dehydration. Intracerebroventricular (icv) administration of prostaglandin D(2) (PGD(2); 20 microg/5 microl) to conscious adult male Sprague-Dawley rats deprived of water for 24 h did not alter significantly the already elevated plasma levels of vasopressin or oxytocin. When PGD(2) was administered in combination with losartan, an antagonist of ANG II AT(1)-receptor subtype, however, concentrations of both hormones in plasma became further elevated. Icv administration of ANG II (50 ng/5 microl) increased further the enhanced plasma levels of vasopressin and oxytocin, as expected. Pretreatment with indomethacin (200 microg/5 microl; icv), an inhibitor of cyclo-oxygenase, significantly attenuated the ANG II-induced increase in oxytocin secretion only. Independent of the presence of ANG II, however, indomethacin decreased plasma levels of vasopressin, but not oxytocin. These results indicate that a prostaglandin is required for the stimulated release of vasopressin during dehydration and that the elevation of oxytocin secretion in response to ANG II depends largely on activation of cyclo-oxygenase and production of prostaglandins. The oxytocin response to exogenously administered PGD(2), however, can be negatively modulated by a mechanism dependent upon ANG II AT(1) receptors.

Indomethacin prevents the L-NAME-induced increase in plasma levels of oxytocin in dehydrated rats.

Inhibiting NO synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME, 250 microg/5 microl of artificial cerebrospinal fluid (aCSF)) injected intracerebroventricularly (i.c.v.) increased already enhanced levels of oxytocin, but not vasopressin, in conscious adult male Sprague-Dawley rats dehydrated for 24 h. Intracerebroventricular pretreatment with indomethacin (200 microg/5 microl aCSF), an inhibitor of cyclo-oxygenase, but not with losartan (25 microg/5 microl aCSF), an antagonist of angiotensin II (ANG II) AT(1)-receptor subtype, nearly prevented the elevation in oxytocin levels after L-NAME. Thus, NO inhibits prostaglandin (but not ANG II) mediated the modulatory actions of NO on oxytocin secretion from the hypothalamo-neurohypophysial system (HNS) during water deprivation.

Centrally produced nitric oxide and the regulation of body fluid and blood pressure homeostases.

1. Nitric oxide (NO) tonically inhibits the basal release of vasopressin and oxytocin into plasma. 2. Nitric oxide inhibition on vasopressin secretion is removed, while that on oxytocin is enhanced, during water deprivation, hypovolaemia, moderate osmotic stimulation and angiotensin (Ang)II. This results in a preferential release of vasopressin over oxytocin that promotes conservation of water. 3. Nitric oxide facilitates drinking behaviour stimulated by water deprivation, osmotic stimulation, haemorrhage and AngII. Together with the hormonal response, NO produces a positive water balance during reductions in intracellular and intravascular volumes. 4. Nitric oxide produced within the central nervous system maintains resting arterial blood pressure partially by attenuating the pressor actions of AngII and prostaglandins. 5. Central production of NO is enhanced during osmotic stimulation to counterbalance the salt-induced pressor response. 6. Paradoxically, central production of NO is also enhanced during haemorrhage, presumably to maintain peripheral vasodilation and blood flow to vital organs.

Angiotensin II does not mediate the pressor response to PGD2 (icv).

The objective of the present studies was to examine the interaction between brain-derived angiotensin II (Ang II) and prostaglandins in order to identify the mechanisms mediating the pressor response produced by these neuroregulators. Inhibiting synthesis of prostaglandins with indomethacin [indocin, 200 microg/ 5 microl artificial cerebrospinal fluid (aCSF)], administered intracerebroventricularly (icv) to conscious adult male Sprague-Dawley rats, reduced blood pressure to values below basal levels. When injected prior to Ang II (50 ng/5 microl aCSF; icv), indomethacin completely abolished the pressor response induced by the octapeptide. The increase in blood pressure produced by prostaglandin D(2) (PGD(2), 20 microg/5 microl; icv), the most prominent prostaglandin in the rat brain, however, was not prevented by losartan (25 microg/5 microl; icv), an Ang II AT(1)-receptor antagonist. Collectively, these results indicate that prostaglandins produced tonically in the brain maintain resting arterial blood pressure and that the pressor action of Ang II is dependent on de novo synthesis of a prostaglandin.

Nitric oxide control of drinking, vasopressin and oxytocin release and blood pressure in dehydrated rats.

Intracerebroventricular (i.c.v.) injection of the inhibitor of NO synthase (NOS), N(G)-nitro-L-arginine methyl ester (L-NAME) (250 microg/5 microL) attenuated the drinking response in rats deprived of water for 24 h. Moreover, oxytocin (OT) levels in plasma increased after 2 min, whereas both oxytocin and vasopressin levels were elevated at 120 min after intracerebroventricular injection. The delayed effect of L-NAME on both hormones was not observed in dehydrated animals allowed to drink water. Blood pressure remained stable after injection of artificial cerebrospinal fluid (aCSF) in dehydrated rats not allowed to drink. In rats having access to water, however, there was an immediate but transient pressor response (0-5 min) with a delayed hypotension from 45 to 120 min. L-NAME consistently increased blood pressure in a biphasic mode, whether the animals drank or not, with an early peak at 5 min that decayed after 15-30 min and a second pressor response beginning at 30-45 min and remaining elevated at 120 min when the experiment ended. These pressor responses were independent of the adrenal glands. Thus, centrally produced nitric oxide facilitates drinking, inhibits release of vasopressin and oxytocin from the magnocellular system, and maintains resting arterial blood pressure in normally hydrated and dehydrated rats.

Brain ANG II and prostaglandins mediate the pressor response after central blockade of nitric oxide synthase.

Central inhibition of nitric oxide synthase (NOS) by intracerebroventricular (i.c.v.) administration of NG-nitro-l-arginine methyl ester (L-NAME; 150 microg/5 microl) to conscious rats produced a biphasic pressor response characterized by an initial transient increase within 5 min, and a delayed response starting between 60-90 min. The effect was stereospecific, as D-NAME (250 microg/5 microl) did not modify the resting arterial blood pressure, nor did L-arginine (323 microg/5 microl, i.c.v.), indicating the substrate for NOS is not rate-limiting. Intracerebroventricular pretreatment with losartan (25 microg/5 microl), a non-peptide antagonist of the angiotensin II AT1 receptor subtype, or indomethacin (100 microg/5 microl), a blocker of cyclooxygenase, however, prevented the initial increase in blood pressure without affecting the delayed pressor response. In contrast, neither intravenous losartan (10 mg/kg b.wt) nor prazosin, an alpha1 adrenergic receptor antagonist, at doses of 5 microg/5 microl (i.c.v.) or 0.3 mg/kg b.wt (i.v.) were effective in altering the pressor responses. These results indicate that centrally produced NO maintains the resting arterial blood pressure at least partially through modulation of the brain angiotensin system and prostaglandins.

Effects of L-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats.

NG-nitro-L-arginine methyl ester (L-NAME; 250 micrograms/5 microliters), an inhibitor of NO synthase, or the vehicle artificial cerebrospinal fluid (aCSF; 5 microliters) was administered intracerebroventricularly to conscious rats hemorrhaged (0.7 ml/min) to a 20% volume depletion. Hypotension was maximal 5 min after hemorrhage ended, with compensatory recovery to basal levels 20 min later, regardless of drug treatment. L-NAME, however, elevated (P < 0.05) blood pressure (vs. aCSF controls) 40-45 min after intracerebroventricular administration. In normovolemic rats, L-NAME produced a significant pressor response and increased plasma levels of vasopressin (VP) and oxytocin (OT). After hemorrhage, both hormone levels increased, but only OT was further enhanced by L-NAME. Thus centrally produced NO tonically inhibits OT and VP secretion under basal normovolemic conditions and selectively inhibits OT release during hypovolemia. Hemorrhage increased the rates of glucose utilization in the neural lobe, indicative of enhanced efferent neural functional activity. L-NAME further enhanced the metabolic activity in the entire hypothalamoneurohypophysial system of hemorrhaged animals. Several other brain structures involved in the regulation of blood pressure and the stress response were also metabolically affected by the hemorrhage and L-NAME.

Effects of central injection of kyotorphin and L-arginine on oxytocin and vasopressin release and blood pressure in conscious rats.

Intracerebroventricular (I.C.V.) administration of an inhibitor of nitric oxide synthase (NOS) increases oxytocin but not vasopressin secretion, in dehydrated rats [38]. Surprisingly, central injection of L-arginine, the substrate for NOS, caused a similar effect. Kyotorphin (L-tyrosyl-L-arginine), a dipeptide formed from L-arginine by kyotorphin synthetase in the brain may mediate this magnocellular response. Therefore, the dose and time responses of hormone release were compared following I.C.V. injection of kyotorphin and L-arginine to conscious rats that were normally hydrated or deprived of water for 24 h. In water-sated rats, both L-arginine and kyotorphin increased blood pressure and plasma glucose levels coincident with elevating circulating levels of oxytocin, but not vasopressin. In dehydrated animals, both L-arginine and kyotorphin increased plasma oxytocin levels with a similar time course but only kyotorphin decreased vasopressin release. D-arginine, like L-arginine, stimulated secretion of oxytocin, indicating a nonstereospecific effect. A kyotorphin receptor antagonist (L-leucyl-L-arginine) given I.C.V. to dehydrated animals elevated plasma oxytocin and prevented the decrease in vasopressin levels after kyotorphin. Thus, kyotorphin, but not L-arginine, appears to attenuate release of vasopressin either directly from magnocellular neurons or indirectly via modulating compensatory reflexes activated by the pressor response. On the other hand, an excess of L-arginine and kyotorphin within the CNS may mimic the stress response by augmenting release of oxytocin and activating the sympathetic nervous system to increase blood pressure and plasma glucose levels.

Effects of chronic central infusion of oxytocin on the response of the magnocellular neuroendocrine system to osmotic stimulation.

The effect of continuous intracerebroventricular (i.c.v.) infusion of oxytocin (OT) on the release of OT and vasopressin (VP) following osmotic stimulation was studied in ovariectomized rats treated peripherally with gonadal steroids to simulate late gestation/lactation. Artificial cerebrospinal fluid (CSF) with or without OT (2 ng/microg) was infused (0.5 microl/h) i.c.v. continuously for 7 days along with sequential peripheral administration of progesterone (2 mg/kg i.m.) for 4 days, then 17-beta-estradiol (200 microg/kg i.m.) for 2 days. Following 7 days of OT infusion, isotonic (0.15 mol/l NaCl) or hypertonic (1.5 mol/l NaCl) saline was injected (15 ml/kg s.c.); the animals were decapitated 1 h later. Animals infused centrally with OT had higher basal levels of OT in plasma (p < 0.01 vs. CSF). While osmotic stimulation increased plasma levels of both OT and VP (0.15 mol/l NaCl < 1.5 mol/l NaCl; p < 0.01), only circulating VP was enhanced further (p < 0.01) in animals infused with OT compared with those receiving CSF. These changes in hormone levels could not be explained by differences in neural lobe stores of OT or VP or by alterations in daily water intake during the infusion period. Thus, chronic i.c.v. infusion of OT stimulates basal release of OT and increases the response of the VP system to osmotic stimulation.

[Refolding of recombinant proteins in vitro].

Refolding of recombinant proteins is an important event in the downstream process of genetic engineering. On the basis of the mechanism of protein folding in vitro, general strategy of recombinant protein refolding is postulated, and major developments in recent years on this field are reviewed, including: molecular chaperone mediated refolding, detergent-assisted refolding, protein refolding in reverse micelle, addition of folding enhancer and methods for the formation of disulfide bond during protein refolding.

Role of NO on vasopressin and oxytocin release and blood pressure responses during osmotic stimulation in rats.

NG-nitro-L-arginine methyl ester (L-NAME, 250 micrograms/5 microliters), an inhibitor of nitric oxide (NO) synthase, or artificial cerebrospinal fluid (5 microliters) was administered intracerebroventricularly to conscious naive rats or to rats treated subcutaneously (15 microliters/kg) with NaCl (0.15, 0.45, or 1.0 M) or given a needle prick only. Intracerebroventricular injection of L-NAME increased plasma concentration of vasopressin (VP) and oxytocin (OT) in control naive rats, indicating that NO tonically inhibits basal secretion of both hormones during isosmotic isovolemic conditions. Osmotic stimulation with hypertonic saline (0.45 and 1.0 M NaCl) elevated plasma levels of both hormones as expected. Central blockade of NO synthase further enhanced secretion of OT during mild, but not strong, osmotic stimulation, whereas the high levels of VP remained unaffected by L-NAME. In animals treated with the needle prick or 0.15 M NaCl, only OT levels were increased after L-NAME. Therefore, NO selectively inhibits OT release in response to a painful stimulus (needle prick) and moderate osmotic stimulation to promote a preferential release of VP. A transient pressor response was observed after subcutaneous injection of 0.15 and 0.45 M NaCl, but a sustained response was obtained after 1.0 M NaCl. Regardless of whether the animals received NaCl solutions, however, treatment with L-NAME elevated blood pressure in all animals. Thus NO-induced vasodilation maintains basal arterial blood pressure and limits the pressor response to osmotic stimulation.

NO and angiotensin II effects on blood pressure and fluid homeostasis.

Angiotensin II (50 ng/5 microl) and L-NAME (250 microg/5 microl), an inhibitor of NO synthase (NOS), were administered intracerebroventricularly alone or in combination to conscious rats. Mean arterial blood pressure (MABP) increased reaching a peak within 5 min in all groups compared to controls treated with the vehicle, artificial CSF (5 microl). MABP returned to basal levels at 30 min after angiotensin II and remained stable for the following 90 min. In animals treated with L-NAME alone, after the initial pressor response, MABP declined but began to increase progressively from 30 min until the end of the experiment at 120 min. When administered with angiotensin II, however, the initial pressor response was prolonged. Angiotensin II-induced drinking was significantly attenuated by L-NAME. In control rats, inhibiting NOS elevated plasma levels of oxytocin and vasopressin but in angiotensin II-stimulated animals, only oxytocin was further elevated after L-NAME. Thus, NO formed centrally inhibits basal secretion of oxytocin and vasopressin as well as the resting blood pressure. During stimulation with angiotensin II, NO facilitates drinking, limits the pressor response and selectively inhibits oxytocin release.

Osmoregulation of the magnocellular neuroendocrine system during lactation.

Glucose utilization and Fos expression were used to compare responses of cerebral structures involved in osmoregulation in virgin and lactating rats given 0.15, 0.85, or 1.5 M NaCl subcutaneously. In virgin animals, glucose utilization increased (P < 0.05) in the supraoptic nuclei (SON), paraventricular nuclei (PVN), and neural lobe (NL) proportionally to the osmotic stimulus (0.15 M NaCl < 0.85 M NaCl < 1.5 M NaCl), whereas metabolism in the median preoptic nucleus (MPO) and median eminence (ME) increased only after 1.5 M NaCl. In lactating rats, enhanced utilization of glucose in response to osmotic stimulation was absent in the PVN (0.85 M NaCl), MPO, and ME or significantly (P < 0.01) reduced (SON, PVN, NL) compared with virgin animals. Glucose utilization in each structure correlated linearly with plasma osmolality but with a lower slope (P < 0.05) in lactating animals. Magnocellular neurons expressing Fos in the SON increased linearly with plasma osmolality and were more numerous (P < 0.05) in control lactating animals but increased less (P < 0.05) than in virgin rats after 0.85 M NaCl. The attenuated magnocellular response during lactation results from reduced afferent activation from osmosensitive forebrain sites.

Expression of transforming growth factor beta in radiation interstitial pneumonitis.

We investigated the changes in transforming growth factor beta 1 (TGF-beta 1) mRNA and TGF-beta 3 protein expression that occur in radiation interstitial pneumonitis. We used TGF-beta 1-cDNA probe in situ hybridization and TGF-beta 3 polyclonal antibody in immunohistochemical techniques. Our results showed that the distribution of TGF-beta 1 mRNA and TGF-beta 3 protein basically coincided in blood vessels, airways, lung parenchyma, and alveolar macrophages. However, bronchial epithelial cells expressed only TGF-beta 3 proteins and no TGF-beta 1 mRNA. We found an increased expression of TGF-beta 1 mRNA and TGF-beta 3 proteins in radiation interstitial pneumonitis.