bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of the medial prefrontal cortex in 5‐HT1A receptor‐induced inhibition of 5‐HT neuronal activity in the rat
Authors: Hajós Mihály , Hajós‐Korcsok Éva , Sharp Trevor 
Published: January 2005

We examined the involvement of the frontal cortex in the 5‐HT1A receptor‐induced inhibition of 5‐HT neurones in the dorsal raphe nucleus (DRN) of the anaesthetized rat using single‐unit recordings complemented by Fos‐immunocytochemistry.
Both transection of the frontal cortex as well as ablation of the medial region of the prefrontal cortex (mPFC) significantly attenuated the inhibition of 5‐HT neurones induced by systemic administration of the 5‐HT1A receptor agonist, 8‐OH‐DPAT (0.5–16 μg kg−1, i.v.). In comparison, the response to 8‐OH‐DPAT was not altered by ablation of the parietal cortex. The inhibitory effect of 8‐OH‐DPAT was reversed by the 5‐HT1A receptor antagonist, WAY 100635 (0.1 mg kg−1, i.v.) in all neurones tested.
In contrast, cortical transection did not alter the sensitivity of 5‐HT neurones to iontophoretic application of 8‐OH‐DPAT into the DRN. Similarly, cortical transection did not alter the sensitivity of 5‐HT neurones to systemic administration of the selective 5‐HT reuptake inhibitor, paroxetine (0.1–0.8 mg kg−1, i.v.).
8‐OH‐DPAT evoked excitation of mPFC neurones at doses (0.5–32 μg kg−1, i.v.) in the range of those which inhibited 5‐HT cell firing. At higher doses (32–512 μg kg−1, i.v.) 8‐OH‐DPAT inhibited mPFC neurones. 8‐OH‐DPAT (0.1 mg kg−1, s.c.) also induced Fos expression in the mPFC. The neuronal excitation and inhibition, as well as the Fos expression, were antagonized by WAY 100635.
These data add further support to the view that the inhibitory effect of 5‐HT1A receptor agonists on the firing activity of DRN 5‐HT neurones involves, in part, activation of a 5‐HT1A receptor‐mediated postsynaptic feedback loop centred on the mPFC.

British Journal of Pharmacology (1999) 126, 1741–1750; doi:10.1038/sj.bjp.0702510
Anti‐inflammatory activity of c(ILDV‐NH(CH2)5CO), a novel, selective, cyclic peptide inhibitor of VLA‐4‐mediated cell adhesion
Authors: Haworth Duncan , Rees Amanda , Alcock Peter J , Wood Linda J , Dutta Anand S , Gormley James J , Jones Huw B , Jamieson Alec , Reilly Christopher F 
Published: January 2005

Small, N‐ to C‐terminal cyclized peptides containing the leucyl‐aspartyl‐valine (LDV) motif from fibronectin connecting segment‐1 (CS‐1) have been investigated for their effects on the adhesion of human T‐lymphoblastic leukaemia cells (MOLT‐4) to human plasma fibronectin in vitro mediated by the integrin Very Late Antigen (VLA)‐4 (α4β1, CD49d/CD29).
Cyclo(‐isoleucyl‐leucyl‐aspartyl‐valyl‐aminohexanoyl‐) (c(ILDV‐NH(CH2)5CO)) was approximately 5 fold more potent (IC50 3.6±0.44 μM) than the 25‐amino acid linear CS‐1 peptide. Cyclic peptides containing two more or one less methylene groups had similar potency to c(ILDV‐NH(CH2)5CO) while a compound containing three less methylene groups, c(ILDV‐NH(CH2)2CO), was inactive at 100 μM.
c(ILDV‐NH(CH2)5CO) had little effect on cell adhesion mediated by two other integrins, VLA‐5 (α5,β1, CD49e/CD29) (K562 cell adhesion to fibronectin) or Leukocyte Function Associated molecule‐1 (LFA‐1, αLβ2, CD11a/CD18) (U937 cell adhesion to Chinese hamster ovary cells transfected with intercellular adhesion molecule‐1) at concentrations up to 300 μM.
c(ILDV‐NH(CH2)5CO) inhibited ovalbumin delayed‐type hypersensitivity or oxazolone contact hypersensitivity in Balb/c mice when dosed continuously from subcutaneous osmotic mini‐pumps (0.1–10 mg kg−1 day−1). Maximum inhibition (approximately 40%) was similar to that caused by the monoclonal antibody PS/2 (7.5 mg kg−1 i.v.) directed against the α4 integrin subunit.
c(ILDV‐NH(CH2)5CO) also inhibited oxazolone contact hypersensitivity when dosed intravenously 20 h after oxazolone challenge (1–10 mg kg−1). Ear swelling was reduced at 3 h and 4 h but not at 1 h and 2 h post‐dose (10 mg kg−1).
Small molecule VLA‐4 inhibitors derived from c(ILDV‐NH(CH2)5CO) may be useful as anti‐inflammatory agents.

British Journal of Pharmacology (1999) 126, 1751–1760; doi:10.1038/sj.bjp.0702511
Respiratory action of capsaicin microinjected into the nucleus of the solitary tract: involvement of vanilloid and tachykinin receptors
Authors: Mazzone Stuart B , Geraghty Dominic P 
Published: January 2005

The respiratory response to microinjection of capsaicin into the commissural nucleus of the solitary tract (cNTS) of urethane‐anaesthetized rats was investigated in the absence and presence of the competitive vanilloid (capsaicin) antagonist, capsazepine, and selective tachykinin NK1, NK2 and NK3 antagonists (RP 67580, SR 48968 and SR 142801, respectively).
Microinjection of capsaicin reduced respiratory frequency but not tidal volume (VT), leading to an overall reduction in minute ventilation (V{dot above}E). The effect was dose‐dependent between 0.5 and 2 nmol capsaicin. Doses greater than 2 nmol produced apnoea. Tachyphylaxis was observed following repeated injection of capsaicin (1 nmol, 30 min apart).
Capsazepine (1 nmol) had no effect on frequency or VT when injected alone but completely blocked the respiratory response to capsaicin (1 nmol).
RP 67580 (1 but not 5 nmol) alone depressed frequency and VT slightly. Moreover, RP 67580 appeared to potentiate the bradypnoeic effect of capsaicin. In contrast, SR 48968 and SR 142801 (1 and 5 nmol) alone had no significant effect on respiration. However, both agents significantly attenuated the reduction in frequency produced by capsaicin.
In conclusion, microinjection of capsaicin into the cNTS decreases overall ventilation, primarily by reducing frequency. The action of capsaicin appears from the data to be mediated by vanilloid receptors since it is blocked by the competitive vanilloid antagonist capsazepine and is subject to tachyphylaxis. However, since NK2 (SR 48968) and NK3 (SR 142801) receptor antagonists block the actions of capsaicin, we propose that capsaicin acts also by releasing tachykinins from central afferent terminals in the cNTS.

British Journal of Pharmacology (1999) 127, 473–481; doi:10.1038/sj.bjp.0702522
The bradykinin B1 receptor and the central regulation of blood pressure in spontaneously hypertensive rats
Authors: Emanueli Costanza , Chao Julie , Regoli Domenico , Chao Lee , Ni Aiguo , Madeddu Paolo 
Published: January 2005

We evaluated if the brain bradykinin (BK) B1 receptor is involved in the regulation of blood pressure (BP) in conscious rats.
Basal mean BP and HR were 115±2 and 165±3 mmHg and 345±10 and 410±14 beats min−1 in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR), respectively. Intracerebroventricular (i.c.v.) injection of 1 nmol B1 receptor agonist Lys‐desArg9‐BK significantly increased the BP of WKY and SHR by 7±1 and 19±2 mmHg, respectively. One nmol Sar[D‐Phe8]‐desArg9‐BK, a kininase‐resistant B1 agonist, increased the BP of WKY and SHR by 19±2 and 17±2 mmHg, respectively and reduced HR in both strains.
I.c.v. injection of 0.01 nmol B1 antagonists, LysLeu8‐desArg9‐BK or AcLys[D‐βNal7,Ile8]‐desArg9‐BK (R715), significantly decreased mean BP in SHR (by 9±2 mmHg the former and 14±3 mmHg the latter compound), but not in WKY. In SHR, the BP response to R715 was associated to tachycardia.
I.c.v. Captopril, a kininase inhibitor, increased the BP of SHR, this response being partially prevented by i.c.v. R715 and reversed into a vasodepressor effect by R715 in combination with the B2 antagonist Icatibant.
I.c.v. antisense oligodeoxynucleotides (ODNs) targeted to the B1 receptor mRNA decreased BP in SHR, but not in WKY. HR was not altered in either strain. Distribution of fluorescein‐conjugated ODNs was detected in brain areas surrounding cerebral ventricles.
Our results indicate that the brain B1 receptor participates in the regulation of BP. Activation of the B1 receptor by kinin metabolites could participate in the pathogenesis of hypertension in SHR.

British Journal of Pharmacology (1999) 126, 1769–1776; doi:10.1038/sj.bjp.0702527
Differential pharmacology between the guinea‐pig and the gorilla 5‐HT1D receptor as probed with isochromans (5‐HT1D‐selective ligands)
Authors: Pregenzer Jeffrey F , Alberts Glen L , Im Wha Bin , Slightom Jerry L , Ennis Michael D , Hoffman Robert L , Ghazal Nabil B , TenBrink Ruth E 
Published: January 2005

Both the 5‐HT1D and 5‐HT1B receptors are implicated in migraine pathophysiology. Recently isochromans have been discovered to bind primate 5‐HT1D receptors with much higher affinity than 5‐HT1B receptors. In the guinea‐pig, a primary animal model for anti‐migraine drug testing, however, isochromans bound the 5‐HT1D receptor with lower affinity than the gorilla receptor.
This species‐specific pharmacology was investigated, using site‐directed mutagenesis on cloned guinea‐pig receptors heterologously expressed in human embryonic kidney 293 cells. Mutations of threonine 100 and arginine 102 at the extracellular side of transmembrane II of the guinea‐pig 5‐HT1D receptor to the corresponding primate residues, isoleucine and histidine, respectively, enhanced its affinity for isochromans to that of the gorilla receptor, with little effects on its affinities for serotonin, sumatriptan and metergoline. Free energy change from the R102H mutation was about twice as much as that from the T100I mutation.
For G protein‐coupling, serotonin marginally enhanced GTPγ35S binding in membranes expressing the guinea‐pig 5‐HT1D receptor and its mutants, but robustly in membranes expressing the gorilla receptor. Sumatriptan enhanced GTPγ35S binding in the latter nearly as much as serotonin, and several isochromans by 30–60% of serotonin.
We discovered key differences in the function and binding properties of guinea‐pig and gorilla 5‐HT1D receptors, and identified contributions of I100 and H102 of primate 5‐HT1D receptors to isochroman binding. Among common experimental animals, only the rabbit shares I100 and H102 with primates, and could be useful for studying isochroman actions in vivo.

British Journal of Pharmacology (1999) 127, 468–472; doi:10.1038/sj.bjp.0702532
Suppressive effect of distinct bradykinin B2 receptor antagonist on allergen‐evoked exudation and leukocyte infiltration in sensitized rats
Authors: Bandeira‐Melo Christianne , Calheiros Andrea S , Silva Patricia M R , Cordeiro Renato S B , Teixeira Mauro M , Martins Marco A 
Published: January 2005

Bradykinin is suggested to play a role in the pathophysiology of several acute and chronic diseases, including allergic disorders such as asthma. In the present study, we have investigated the importance of bradykinin in mediating allergic inflammation in rats.
To this end we have tested the effects of the B2 receptor antagonists Hoe 140, FR173657 or FR172357 on the pleural inflammatory response triggered by intrapleural (i.pl.) injection of allergen (ovalbumin, 12 μg cavity−1) in 14 day‐actively sensitized Wistar rats. Analysis of the pleural fluid effluent revealed a sequence of mast cell‐dependent inflammatory events, including early protein exudation and neutrophilia and late pleural eosinophil influx.
Local treatment with Hoe 140 (0.1 and 1 μg cavity−1), FR173657 (1 and 10 μg cavity−1) or FR172357 (1 and 10 μg cavity−1) inhibited dose‐dependently allergen‐induced mast cell activation with impairment of pleural plasma leakage, neutrophil accumulation and late eosinophil influx.
Moreover, the B2 receptor antagonists also dose‐dependently inhibited the allergic like inflammatory pleurisy triggered by bradykinin (50 μg cavity−1), which is characterized by acute mast cell degranulation, protein leakage and pleural eosinophil infiltration.
Taken together, our findings provide substantial evidence to suggest that bradykinin acting on its B2 receptors play a critical role in mediating allergic mast cell‐dependent inflammation in rats, and suggest that B2 receptor antagonists may be useful therapeutically to control allergic dysfunction.

British Journal of Pharmacology (1999) 127, 315–320; doi:10.1038/sj.bjp.0702536
Tonic inhibitory action by nitric oxide on spontaneous mechanical activity in rat proximal colon: involvement of cyclic GMP and apamin‐sensitive K+ channels
Authors: Mulè F , D'Angelo S , Serio R 
Published: January 2005

The cellular mechanisms by which endogenous nitric oxide (NO) modulates spontaneous motility were investigated in rat isolated proximal colon. The mechanical activity was detected as changes in intraluminal pressure.
Apamin (1–100 nM) produced a concentration‐dependent increase in the amplitude of the spontaneous pressure waves. The maximal contractile effect was of the same degree as that produced by Nω‐nitro‐L‐arginine methyl ester (L‐NAME) (100 μM) and the joint application of apamin plus L‐NAME had no additive effects. Apamin (0.1 μM) reduced the inhibitory effects (i.e. reduction in the amplitude of the pressure waves) induced by sodium nitroprusside (SNP) (1 nM–10 μM) or 8‐Br‐cyclic GMP (1–100 μM).
1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ) (0.1–5 μM), inhibitor of NO‐stimulated guanylate cyclase, produced a concentration‐dependent increase of the spontaneous contractions. ODQ (1 μM) in the presence of apamin (0.1 μM) did not produce any further increase in the contraction amplitude, whereas after L‐NAME (100 μM) it decreased the spontaneous contractions. ODQ (1 μM) reduced the SNP inhibitory effects.
Zaprinast (1–50 μM), inhibitor of cyclic GMP phosphodiesterase, produced a concentration‐dependent decrease of the spontaneous contractions. The effects of zaprinast were significantly reduced in the presence of apamin (0.1 μM) or L‐NAME (100 μM).
These results suggest that small conductance Ca2+‐dependent K+ channels and cyclic GMP are involved in the modulation of the spontaneous contractile activity in rat proximal colon. Cyclic GMP production system and opening of apamin‐sensitive K+ channels appear to work sequentially in transducing an endogenous NO signal.

British Journal of Pharmacology (1999) 127, 514–520; doi:10.1038/sj.bjp.0702537
Effects of mitoxantrone on action potential and membrane currents in isolated cardiac myocytes
Authors: Wang Ge‐Xin , Zhou Xiao‐Bo , Eschenhagen Thomas , Korth Michael 
Published: January 2005

The effects of mitoxantrone (MTO), an anticancer drug, on the membrane electrical properties of cardiac myocytes were investigated using the whole‐cell clamp technique.
In isolated guinea‐pig ventricular myocytes, 30 μM MTO induced a time‐dependent prolongation of action potential duration (APD) which was occasionally accompanied by early afterdepolarizations. APD prolongation was preserved in the presence of 10 μM tetrodotoxin and showed reverse rate‐dependence.
Both the inward rectifier K+ current (IK1) and the delayed rectifier K+ current (IK) of guinea‐pig ventricular myocytes were significantly depressed by 30 μM MTO. The rapidly activating component of IK (IKr) seemed to be preferentially blocked by MTO. The transient outward current was not affected by MTO in rat ventricular myocytes.
Thirty μM MTO had no direct effect on the L‐type Ca2+ current (ICa(L)), but reversed the inhibitory effect of 1 μM carbamylcholine but not the A1‐adenosine receptor agonist (−)‐N6‐phenylisopropyladenosine (1 μM) on ICa(L) enhanced by 50 nM isoprenaline in guinea‐pig ventricular myocytes. In guinea‐pig atrial mycotyes, 30 μM MTO inhibited by 93% the muscarinic receptor gated K+ current (IK,ACh) evoked by 1 μM carbamylcholine, whereas IK,ACh elicited by 100 μM GTPγS, a nonhydrolysable GTP analogue, was only decreased by 12%.
The specific binding of [3H]QNB, a muscarinic receptor ligand, to human atrial membranes was concentration‐dependently displaced by MTO (1–1000 μM).
In conclusion, MTO blocks cardiac muscarinic receptors and prolongs APD by inhibition of IK1 and IKr. The occasionally observed early afterdepolarizations may signify a potential cardiac hazard of the drug.

British Journal of Pharmacology (1999) 127, 321–330; doi:10.1038/sj.bjp.0702547
The attenuation of learning impairments induced after exposure to CO or trimethyltin in mice by sigma (σ) receptor ligands involves both σ1 and σ2 sites
Authors: Maurice Tangui , Phan Vân‐Ly , Noda Yukihiro , Yamada Kiyofumi , Privat Alain , Nabeshima Toshitaka 
Published: January 2005

Sigma (σ) receptor ligands were previously reported to alleviate learning and memory impairments on several pharmacological and pathological rodent models of amnesia. Such effect was demonstrated as involving the σ1 subtype of σ receptor.
In this study, we characterized the pharmacological effect mediated by σ ligands on two lesional models of amnesia in mice: (1) the hypoxia‐related learning and memory impairment model induced by repeated exposure to carbon monoxide (CO) gas; and (2) the intoxication with trimethyltin (1 mg kg−1).
The selective σ1 ligand PRE‐084 (1 mg kg−1) or the non‐selective σ1/σ2 compounds DTG (0.1 mg kg−1), BD1008 (3 mg kg−1), and haloperidol (0.1 mg kg−1) reversed significantly the spontaneous alternation deficits observed 7 days after exposure to CO or 14 days after intoxication with trimethyltin.
The selective σ1 receptor antagonist NE‐100 (1 mg kg−1) was ineffective by itself, but blocked completely the PRE‐084 effects, partially the DTG effects, and did not affect the effects induced by BD1008 or haloperidol.
A similar pharmacological profile was observed in the step‐down type passive avoidance test performed 8 days after exposure to CO.
These results show that, in contrast to the previously reported amnesia models, the impairments induced after exposure to CO or intoxication with trimethyltin could be alleviated not only by σ1 receptor agonists but also by σ2 agonists. The particular pattern of neurodegeneration observed in these lesional models may explain these differences.

British Journal of Pharmacology (1999) 127, 335–342; doi:10.1038/sj.bjp.0702553
Parallel modulation of receptor for activated C kinase 1 and protein kinase C‐α and β isoforms in brains of morphine‐treated rats
Authors: Escribá Pablo V , García‐Sevilla Jesús A 
Published: January 2005

Receptor for activated C kinase 1 (RACK1) is an intracellular receptor for protein kinase C (PKC) that regulates the cellular enzyme localization. Because opiate drugs modulate the levels of brain PKC (Ventayol et al., 1997), the aim of this study was to assess in parallel the effects of morphine on RACK1 and PKC‐α and β isozymes densities in rat brain frontal cortex by immunoblot assays.
Acute morphine (30 mg kg−1, i.p., 2 h) induced significant increases in the densities of RACK1 (33%), PKC‐α (35%) and PKC‐β (23%). In contrast, chronic morphine (10–100 mg kg−1, i.p., 5 days) induced a decrease in RACK1 levels (22%), paralleled by decreases in the levels of PKC‐α (16%) and PKC‐β (16%).
Spontaneous (48 h) and naloxone (2 mg kg−1, i.p., 2 h)‐precipitated morphine withdrawal after chronic morphine induced marked up‐regulations in the levels of RACK1 (38–41%), PKC‐α (51–52%) and PKC‐β (48–62%).
In the same brains and for all combined treatments, there were significant positive correlations between the density of RACK1 and those of PKC‐α (r=0.85, n=35) and PKC‐β (r=0.75, n=32).
These data indicate that RACK1 is involved in the short‐ and long‐term effects of morphine and in opiate withdrawal, and that RACK1 modulation by morphine or its withdrawal is parallel to those of PKC‐α and β isozymes. Since RACK1 facilitates the PKC substrate accessibility, driving its cellular localization, the coordinate regulation of the PKC/RACK system by morphine could be a relevant molecular mechanism in opiate addiction.

British Journal of Pharmacology (1999) 127, 343–348; doi:10.1038/sj.bjp.0702555
Endothelium is required in the vascular spasm induced by tetraethylammonium and endothelin‐1 in guinea‐pig aorta
Authors: Dorigo P , Maragno I , Santostasi G , Fraccarollo D 
Published: January 2005

To investigate the role of endothelium in vascular spasm, we studied the influence of endothelin‐1 (ET‐1) on the contracting and spasmogenic effect of the K+‐channel blocker, tetraethylammonium (TEA), in aorta rings of reserpine‐treated guinea‐pigs, perfused with either control (5.5 mM) or elevated (50 mM) glucose concentration.
Endothelium‐dependent relaxation induced by acetylcholine was lost in rings contracted by noradrenaline in the presence of elevated glucose. In control medium, TEA (1–20 mM) induced a sustained tonic contraction, followed by a phasic spasm, characterized by rhythmic contractions. Elevated glucose, ET‐1 (3 nM), or both, reduced the EC50 of TEA‐induced tonic contraction, without modifying the maximum contractile effect.
In control medium, ET‐1 reduced the time before TEA‐induced spasm and increased the rate of rhythmic contractions. TEA‐induced spasm was abolished by elevated glucose, and restored by ET‐1. The spasm induced by TEA and ET‐1 was amplified by the ETA antagonist, EMD94246, and suppressed by the ETA‐ETB antagonist, bosentan. In endothelium‐denuded vessels incubated with high glucose and ET‐1, TEA evoked only a tonic contraction.
In control medium, L‐NAME (NG‐nitro‐L‐arginine methyl ester) abolished TEA‐induced rhythmic contractions. L‐arginine, but not D‐arginine, prevented the effect of L‐NAME. In the presence of elevated glucose and ET‐1, TEA‐induced spasm was not affected by L‐NAME, whereas verapamil, indomethacin, metyrapone, glybenclamide or apamin abolished the phasic spasm, unmasking the tonic contracture.
In conclusion, endothelium plays a regulatory role in the genesis and maintenance of TEA‐induced rhythmic contractions, through the release endothelium derived relaxing factor and vasodilating eicosanoids.

British Journal of Pharmacology (1999) 127, 505–513; doi:10.1038/sj.bjp.0702557
Cyclic AMP suppresses interleukin‐5 synthesis by human helper T cells via the downregulation of the calcium mobilization pathway
Authors: Kaminuma Osamu , Mori Akio , Ogawa Koji , Kikkawa Hideo , Nakata Aya , Ikezawa Katsuo , Okudaira Hirokazu 
Published: January 2005

To delineate the mechanism by which cyclic AMP (cAMP) suppresses interleukin (IL)‐5 synthesis, the effects of prostaglandin (PG) E2, forskolin, dibutyryl (db)‐cAMP and the Ca2+ ionophore, ionomycin on cytokine synthesis, proliferation and CD25 expression of human T cells were investigated. Further studies were performed by measurement of the intracellular concentrations of cyclic AMP ([cAMP]i) and Ca2+ ([Ca2+]i) and by electrophoretic mobility shift analysis (EMSA).
PGE2, forskolin and db‐cAMP suppressed IL‐5 production by human T cell line following T cell receptor (TCR)‐stimulation. PGE2 suppressed TCR‐induced messenger RNA (mRNA) expression of IL‐2, IL‐4 and IL‐5, as well as proliferation and CD25 expression.
Cyclic AMP‐mediated suppression of cytokine synthesis, proliferation and CD25 expression in human T cells were attenuated by ionomycin.
[cAMP]i was increased by PGE2 and forskolin. PGE2 suppressed the TCR‐induced biphasic increase in [Ca2+]i. EMSA revealed that four specific protein‐DNA binding complexes related to NF‐AT were detected at the IL‐5 promoter sequence located from −119 to −90 relative to the transcription initiation site. The slowest migrating complex induced by TCR stimulation was enhanced by PGE2 and further upregulated by ionomycin. Another binding which did not compete with cold AP‐1 oligonucleotides, was constitutively present and was unaffected by PGE2 but enhanced by ionomycin.
The suppressive effect of cyclic AMP on human IL‐5 synthesis is mediated by interference with intracellular Ca2+ mobilization but distinct from the NF‐AT‐related pathway.

British Journal of Pharmacology (1999) 127, 521–529; doi:10.1038/sj.bjp.0702558