BACKGROUND: Sliding cupping has been used for treating cervical spondylosis, with the effects of dredging the meridian system, activating qi and removing blood stasis.OBJECTIVE: To probe into symptomatic improvement of cervical spondylosis with sliding cupping and the relationship between curative effect and course of disease as well as age.DESIGN: Self controlled observation.SETTING: Department of Physiotherapy, General Hospital of Air Force of Chinese PLA.PARTICIPANTS: Totally 100 out-patients with cervical spondylosis receiving treatment in the Department of Physiotherapy, General Hospital of Air Force of Chinese PLA were involved from December 2000 to December 2003. Among them, 39 cases were male and 61 cases were female; 9 cases were under 30 years old, 38 cases were 31 to 40 years old, 42 cases were 41 to 50 years old and 11 cases were above 50 years old. There were 36 cases with less-than-one-year course of disease, 49 with 1 to 5-year course and 15 with more-than-5-year course. Fifty-one cases were cervical type; 25 cases vertebral artery type; 24 cases nerve root type. X-ray examination revealed that there were 69 cases whose cervical vertebral physiological curvature became straight or reverse, or with certain degree of degenerative change. Vertebroarterial blood supply insufficiency was detected in 23 cases by rheoencephalogram.INTERVENTIONS: The patients were asked to be in prone sitting position,their nape and shoulder were fully exposed, and the negative pressure cupping was applied to patient' s nape and shoulder until petechiae appeared on the skin. The treatment was given once or twice a week. After one-month treatment, the curative effect was calculated according to subjective symptoms, signs, and the results of X-ray and rheoencephalogram examination before and after treatment. Symptom disappearance: pain was 0 grade; the cervical vertebral physiological curvature restored by 10°- 15° and rheoencephalogram showed that the contraction peak velocity of the vertebroarterial blood supply became normal. Marked improvement: the pain reduced by more than 2 grade, the cervical vertebral physiological curvature restored by 6°9° and rheoencephalogram showed that the vertebroarterial blood supply restored to 80% of the normal range. Improvement: the pain reduced by 1 grade, the cervical vertebral physiological curvature restored by 3°- 5° and rheoencephalogram showed that the vertebroarterial blood supply restored to 40% - 80% of the normal range. Inefficacy: the pain did not reduce, the cervical vertebral physiological curvature restored by less than 3° and rheoencephalogram showed that the vertebroarterial blood supply became less than 40%.RESULTS: According to the intention-to-treat analysis, 100 patients entered the result analysis. For symptom disappearance, marked improvement,improvement, inefficacy there were 27, 17, 5 and 2 cases respectively in cervical type; 8, 10,4 and 3 cases respectively in the vertebral artery type;4,9,7 and 4 cases respectively in the nerve root type. There were 19, 12, 3 and 2 cases respectively with less-than-one-year course of disease; 18, 19, 7 and 5 cases respectively with 1 to 5-year course; 2, 5, 6 and 2 cases respectively with more-than-5-year course. And there were 5, 3 and 1 cases respectively with age ＜ 30 years; 18, 13, 4 and 3 cases respectively with age of 31 to 40 years; 15, 18, 5 and 4 cases respectively with age of 41 to 50years; 1, 2, 6 and 2 cases respectively with age ＞ 50 years.CONCLUSION: The effect of sliding cupping was good for patients with cervical spondylosis of vertical type, next of vertebroarterial type and bad of nerve root type. The shorter the course of disease is, the younger the patient is, and the better the curative effect is.

Objective: To explore the role of angiotensin receptor type I (AT1)-calcineurin (CaN) signaling pathway in transient outward potassium ion channel (Ito) remolding in hypertrophic atrial myocytes of neonatal rats. Methods: 1 day old neonatal rats’ atrial myocytes were isolated and the cells were divided into 4 groups:①Control group, normal cells were cultured for 24 h,②Stretching group, the cells were cultured for 24 h with mechanical stretching to induce hypertrophy,③Telmisartan group, the cells were treated by telmisartan at 1 μmol/L for 1 h, then cultured for 24 h and ④Cyclosporin-A (CsA) group, the cells were treated by CsA at 0.25 μg/ml for 1 h, then cultured for 24 h. The ratios of protein/DNA in myocytes were compared between Control group and Stretching group, cell hypertrophy was deifned by mRNA expression of atrial natriuretic peptide (ANP). Ito changes were detected by whole-cell patch clamping technique, proteins expressions of Kv4.3 and CaN A subunit were examined by Western blot analysis. Results: Compared with Control group, Stretching group showed obviously decreased Ito density and Kv4.3 protein expression, while increased CaN A protein expression; Compared with Stretching group, the above effects were reduced in Telmisartan group and CsA group. Conclusion: AT1-CaN signaling pathway was involved in the regulation of Ito channel remodeling in hypertrophic atrial myocytes of neonatal rats.

AIM:To investigate the effect of angiotensin II type 1 receptor (AT1R)-calcineurin (CaN) signa-ling pathway on the expression of sodium current channel Nav 1.5 at mRNA and protein levels in the hypertrophic ventricu-lar myocytes from neonatal rats .METHODS:The ventricular myocytes were isolated from the ventricles of 1-day-old neo-natal Sprague-Dawley rats and were divided into 4 groups according to different drug intervention as control group , pheny-lephrine (PE) group, losartan (Los)+PE group and cyclosporin A (CsA)+PE group.The method of RNA interference mediated by adenovirus carrying short hairpin RNA ( shRNA) was used to knock down the gene which encodes the beta subtype of CaN A subunit (CnAβ) and the cells were divided into 4 groups as Ad-Null group, Ad-Null+PE group, Ad-CnAβshRNA1 group and Ad-CnAβshRNA1+PE group.The mRNA expression of brain natriuretic peptide ( BNP) ,β-my-osin heavy chain (β-MHC) and Nav1.5 was detected by RT-qPCR.The protein levels of CnAβand Nav1.5 in the whole-cell extracts were determined by Western blot analysis .RESULTS:Treatment of the neonatal rat ventricular myocytes with PE for 24 h increased the protein-to-DNA ratio and the mRNA expression of BNP and β-MHC.The size of the cell surface was also increased after PE treatment .Treatment of the cells with PE increased the protein expression of CnAβ, and re-duced the protein expression of Nav 1.5.Both Los and CsA prevented those effects of PE .The mRNA expression of Nav1.5 was reduced by PE , and no significant difference of Nav 1.5 mRNA expression among PE group , Los+PE group and CsA+PE group was observed .Silencing of CnAβin the neonatal rat ventricular myocytes using Ad-CnAβshRNA1 inhibited the ability of PE to increase the mRNA expression of BNP , and diminished the ability of PE to reduce the protein expression of Nav1.5.CONCLUSION:AT1 R-CaN signaling pathway participates in regulating protein expression of Nav 1.5 in the hy-pertrophic ventricular myocytes from neonatal rats .

Objective Gitelman Syndrome is a disease caused by the mutation of Na-Cl cotransporter gene(SLC12A3).The article studied the significance of diagnosis and identification by genetic mutation. Methods We collected the clinical data, then we sequenced the SLC12A3 gene by the first sequencing technology and MLPA. Results SLC12A3 complicated heterozygotic mutation was observed.One of them showed c.1964G>A, p.(Arg655His) and exon 8 deletion mutation, the other showed c.2543A>T, p.(Asp848Val) and c.976delG, p.(Val326fs) mutation of SLC12A3 gene in children. Conclusion The final diagnosis depended on gene diagnosis. Pediatrician must recognize the manifestations to advoid misdiagnosis.

Objective To evaluate the effect of propofol postconditioning on necroptosis during hy-poxia-reoxygenation (H∕R) injury in diabetic cardiomyocytes. Methods Normally cultured H9C2 cardio-myocytes were divided into 5 groups (n= 19 each) using a random number table: control group (group C), high glucose group (group HG), H∕R group, propofol postconditioning (group P) and solvent dimethyl sulfoxide (DMSO) control group (group DMSO). H9C2 cells were incubated for 48 h in DMEM culture medium containing 5. 5 and 25 mmol∕L glucose in group C and group HG, respectively. In group H∕R, H9C2 cells were incubated for 48 h in DMEM culture medium containing 25 mmol∕L glucose and then un-derwent H∕R. H9C2 cells were incubated for 48 h in DMEM culture medium containing 25 mmol∕L glucose and then underwent H∕R, and propofol at the final concentration of 50 μmol∕L was added at the onset of reoxygenation in group P. In group DMSO, H9C2 cells were incubated for 48 h in DMEM culture medium containing 25 mmol∕L glucose and then underwent H∕R, and DMSO at the final concentration of 150μmol∕L was added at the onset of reoxygenation. The model of cardiomyocyte H∕R injury was established by subjecting cardiomyocytes to 6 h of hypoxia followed by 12 h of reoxygenation. At 12 h of reoxygenation, the cell viability was measured by CCK8 assay, the product of lactate dehydrogenase (LDH) in culture medium was measured, the level of reactive oxygen species (ROS) was determined by flow cytometry, cardiomyo-cyte apoptosis was detected by TUNEL, and the expression of receptor-interacting protein 1 ( RIP1), RIP3, Bax, Bcl-2, activated caspase-3 and caspase-3 was determined by Western blot. The apoptotic rate and ratio of activated caspase-3∕caspase-3 were calculated. Results Compared with group C, the cell via-bility was significantly decreased, the product of LDH was increased, the level of ROS and apoptotic rate were increased, the expression of RIP1, RIP3 and Bax was up-regulated, the expression of Bcl-2 was down-regulated, and the ratio of activated caspase-3∕caspase-3 was increased in group HG ( P < 0. 05). Compared with group HG, the cell viability was significantly decreased, the product of LDH was increased, the level of ROS and apoptotic rate were increased, the expression of RIP1, RIP3 and Bax was up-regula-ted, the expression of Bcl-2 was down-regulated, and the ratio of activated caspase-3∕caspase-3 was in-creased in group H∕R (P<0. 05). Compared with group H∕R, the cell viability was significantly increased, the product of LDH was decreased, the level of ROS and apoptotic rate were decreased, the expression of RIP1, RIP3 and Bax was down-regulated, the expression of Bcl-2 was up-regulated, and the ratio of acti-vated caspase-3∕caspase-3 was decreased in group P (P<0. 05), and no significant change was found in the indexes mentioned above in group DMSO (P>0. 05). Conclusion The mechanism by which propofol post-conditioning ameliorates H∕R injury in diabetic cardiomyocytes may be related to inhibiting necroptosis.

Objective To explore the effect of circ_0038467 on angiotensin Ⅱ(Ang Ⅱ)-induced cardiomyocyte damage and its possible mechanism.Methods Ang Ⅱ was used to induce rat cardiomyocyte H9C2 to establish a cell injury model.si-NC,si-circ_0038467,miR-NC,miR-495 mimics were transfected into H9C2 cells and then treated with 1 μmol/L Ang Ⅱ for 24 h.si-circ_0038467 and anti-miR-NC,si-circ_0038467 and anti-miR-495 were co-transfected into H9C2 cells and treated with 1 μmol/L Ang Ⅱ for 24 h.qRT-PCR method was used to detect the expression levels of circ_0038467 and miR-495.A kit was used to detect the level of MDA and the activity of LDH and SOD.Flow cytometry was used to detect the rate of apoptosis.The dual lu-ciferase reporter experiment was used to detect the targeting relationship between circ_0038467 and miR-495.Western blot was used to detect the protein expression of cleaved Caspase-3 and cleaved Caspase-9,Bcl-2,p-P65 and p-IKBa.Results The expres-sion of circ_0038467 in H9C2 cells induced by Ang Ⅱ was increased(P＜0.05),while the expression of miR-495 was decreased(P＜0.05).After transfection of si-circ_0038467 or miR-495 mimics,the activity of LDH and the level of MDA were decreased(all P＜0.05),the rate of apoptosis and the protein levels of cleaved Caspase-3,cleaved Caspase-9 were decreased(all P＜0.05),while the activity of SOD was increased(P＜0.05).Circ_0038467 could target miR-495.Co-transfection of si-circ_0038467 and anti-miR-495 could antagonize the effect of si-circ_0038467 on Ang Ⅱ-induced oxidative stress and apoptosis of H9C2 cells.In addition,circ_0038467 could activate the NF-κB pathway by targeting miR-495.Conclusion circ_0038467 regu-lates oxidative stress and apoptosis of cardiomyocytes by targeting miR-495/NF-KB pathway.

Hip fractures are among the most common fractures in the elderly, presenting to be a leading cause of disability and mortality. Surgical treatment is currently the main treatment method for hip fractures. The incidence of perioperative malnutrition is increased after hip fractures in the elderly due to the comorbidities, decreased basal metabolic rate, accelerated protein breakdown, weakened anabolism and surgical stress. However, malnutrition not only increases the incidence of postoperative complications, but also leads to increased mortality, indicating an important role of perioperative nursing management of nutrition for the elderly patients with hip fractures. At present, there still lacks scientific guidance and application standards on perioperative nursing management of nutrition for the elderly patients with hip fractures. Therefore, the Orthopedic Nursing Committee of Chinese Nursing Association and the Editorial Board of Chinese Journal of Trauma organized relevant experts to formulate the Expert consensus on perioperative nursing management of nutrition for elderly patients with hip fractures ( version 2023) according to evidence-based medical evidences and their clinical experiences. Fourteen recommendations were made from aspects of nutrition screening, nutrition assessment, nutrition diagnosis, nutrition intervention and nutrition monitoring to provide guidance for perioperative nursing management of nutrition in elderly patients with hip fractures.