OBJECTIVE: To determine if greater efficacy could be achieved with the intranasal antihistamine azelastine and the intranasal corticosteroid fluticasone propionate used concurrently in the treatment of nasal obstruction of persistent non-allergic rhinitis. METHOD: A total of 162 persistent non-allergic rhinitis cases with moderate to severe nasal obstruction were randomized to treatment with the following: the combination therapy or nasal corticosteroids monotherapy. Efficacy was assessed by change from baseline in nasal obstruction score at week 2 and week 6 visits. The perceptions of global treatment satisfaction(convenience, side effects, cost and effectiveness) in both groups were analyzed. RESULT: In both groups, the nasal obstruction score assessment descended significantly at week 2 and week 6 visits versus at baseline (all P < 0.01). At week 2 and week 6 visits, the nasal obstruction score in the combination therapy groups were significantly improved than that in nasal corticosteroids monotherapy groups (all P < 0.01). The perceptions of global treatment satisfaction in the combination therapy groups were significantly better (P < 0.05). CONCLUSION Azelastine nasal spray and intranasal corticosteroid in combination may provide a substantial therapeutic benefit for patients with persistent non-allergic rhinitis, especially nasal obstruction. The combination therapy was well tolerated and safety.
Administration, Intranasal ; Adrenal Cortex Hormones ; therapeutic use ; Drug Therapy, Combination ; Histamine H1 Antagonists ; therapeutic use ; Humans ; Nasal Obstruction ; Phthalazines ; therapeutic use ; Rhinitis ; drug therapy

Objective To modify the method of gavage administration in guinea pigs. Methods Fourty awake guinea pigs were kept rearing on the hind legs and leaning on a vertical fixture to avoid their escaping forward. A 1 mL injector was inserted into the mouth to the depth when the molar teeth were passed. Another fourty guinea pigs under general anesthesia were reversed at trendelenburg position and a children suction tube with an outer diameter of 2 mm was inserted into the stomach. Results All of the 80 guinea pigs were administered by modified gavage smoothly for seven consecutive days by one operator each time. None endured much pain or digestive tract injury, or died from air way perfusion by mistake. Conclusions We successfully modified the gavage method in guinea pigs, which would definitely take guinea pigs involved in intragastical pharmacal experiments besides the routine of rats and mice.

Objective To explore how medical staff in the oncology department understand management of cancer related fatigue (CRF), and explore what factors influencing the effective practice of CRF management. Methods Qualitative inquiry was adopted. Ten medical staffs in the oncology department were selected for in- depth interview. Generic analysis was applied to code, categorize and interpret the qualitative data. Results Participants believed that many factors influenced the CRF, which hadn′t been assessed as an independent symptom and lacked the systematic, effective and specific interventions. The medical staff, patients and their families neglecting the CRF management was the main barrier. Strengthening system construction and staff training was mentioned as major area which needed to be improved. Conclusions CRF management guideline should be formulated according to our national situations based on the clinical practices, besides, the training of correlated clinical knowledge and skills of medical staff should be strengthened and eventually promote the cancer patients′quality of life.

OBJECTIVE: To explore the distribution of cells infected by AD5-EGFP infused in different ways in the cochlea of guinea pig. METHOD: AD5-EGFP was infused into the endolymphatic system through a hole on the lateral wall of the scala media or into the extralymphatic system through the round window membrane respectively. The infected cochlear cells confirmed by expression of EGFP were examined on the whole mount or cryostat sections. RESULT: In the cochleae in which AD5-EGFP was infused into the extralymphatic system through the round window membrane, expression of EFGP could be found in the type I, IV and V fibrocyte of the stria vascularis, superlimbal cells of the spiral lip, cells in Ressenal membrane, spiral ganglion neurons in Rosenthal hole and cells lining the inner wall of scala vestibular and scala tympani, indicating that these cells were infected by adenovirus. None of the inner, outer hair or supporting cells was found to be infected in these cochleae. In the cochleae in which AD5-EGFP was infused into the endolymphatic system through a hole on the lateral wall of scala media, expression of EFGP could be found in supporting cells in the organ of Corti and lining cells of the scala media. CONCLUSION Adenovirus5 is a good and effective vector for delivering genes into cells in guinea pig's cochlea. The scope of infected cells will be very different when the vector is applied to the cochlea through different infusion ways. No cells in the endolymphatic system would be infected if the vector is infused into the extralymphatic system.
Adenoviridae ; genetics ; Animals ; Cochlea ; virology ; Gene Transfer Techniques ; Genes, Reporter ; Genetic Vectors ; Green Fluorescent Proteins ; genetics ; Guinea Pigs ; Spiral Ganglion ; virology

Objective To investigate the mechanisms of paeoniflorin in protection of retinal ischemia injury.Methods Fifty-four male specefic pathogen free (SPF) degree Wistar rats were randomly divided into normal control group,model control group and paeoniflorin group.Retinal ischemia injury was induced by raising the intraocular pressure of right eyes of rats to 110 mmHg for 30 minutes.The rats of paeoniflorin group were administrated through intraperitoneal injection of 5 mg/kg paeoniflorin each day for 14 days.OCT and electroretinogram (ERG) were performed to detect the thickness of retinal nerve fiber layer+retinal ganglion cell layer+inner plexiform layer (NGI)and electrophysiological changes of retina,respectively.Retrograde labelling of retinal ganglion cells (RGCs) was used to evaluate the survival number of RGCs.Western blot analysis was used to detect NLRP3,apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC),cleaved caspase 1 (c-caspase 1),IL-18,and IL-1β expression.The use and care of animals complied with the statement of the Association for Research in Vision and Ophthalmology (ARVO) and Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.Results The thickness of retinal NGI in model control group was (58.2 ± 1.7) μm,which was significantly lower than (84.8 ± 1.9) μm in normal control group and (71.1 ±2.4) μm in paeoniflorin group (both at P＜0.05).The amplitudes of A and B waves in paeoniflorin group and normal control group were significantly higher than those in model control group (both at P＜0.05).The number of RGC in model control group was significantly lower than that in paeoniflorin group and normal control group (both at P＜0.05).The relative expressions of NLRP3,ASC,c-caspase 1,IL-18 and IL-1β in model control group were significantly higher than those in normal control group and paeoniflorin group (all at P＜0.05).Conclusions The paeoniflorin can prevent retinal ischemia induced injury of the retina through NLRP3 inflammasomes pathway,which provides a new treatment strategy for clinical therapy.

Objective To investigate the mechanisms of paeoniflorin in protection of retinal ischemia injury. Methods Fifty.four male specefic pathogen free ( SPF) degree Wistar rats were randomly divided into normal control group,model control group and paeoniflorin group. Retinal ischemia injury was induced by raising the intraocular pressure of right eyes of rats to 110 mmHg for 30 minutes. The rats of paeoniflorin group were administrated through intraperitoneal injection of 5 mg/kg paeoniflorin each day for 14 days. OCT and electroretinogram ( ERG ) were performed to detect the thickness of retinal nerve fiber layer+retinal ganglion cell layer+inner plexiform layer ( NGI) and electrophysiological changes of retina, respectively. Retrograde labelling of retinal ganglion cells ( RGCs ) was used to evaluate the survival number of RGCs. Western blot analysis was used to detect NLRP3,apoptosis.associated speck.like protein containing a caspase activation and recruitment domain (ASC),cleaved caspase 1 (c.caspase 1), IL.18,and IL.1β expression. The use and care of animals complied with the statement of the Association for Research in Vision and Ophthalmology ( ARVO ) and Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results The thickness of retinal NGI in model control group was ( 58. 2 ± 1. 7)μm, which was significantly lower than ( 84. 8 ± 1. 9)μm in normal control group and(71. 1±2. 4)μm in paeoniflorin group (both at P<0. 05). The amplitudes of A and B waves in paeoniflorin group and normal control group were significantly higher than those in model control group ( both at P<0. 05 ) . The number of RGC in model control group was significantly lower than that in paeoniflorin group and normal control group ( both at P<0. 05). The relative expressions of NLRP3,ASC,c.caspase 1,IL.18 and IL.1β in model control group were significantly higher than those in normal control group and paeoniflorin group (all at P<0. 05). Conclusions The paeoniflorin can prevent retinal ischemia induced injury of the retina through NLRP3 inflammasomes pathway,which provides a new treatment strategy for clinical therapy.

OBJECTIVE: To explore whether the Ad5-atoh1/EGFP could transdifferent the supporting cells into the new hair cells in young adult guinea pigs cochlea in vivo. METHOD: Twelve healthy pigmented guinea pigs weighted 200-250 g were included in this experiment. 5 ul of Ad5-E1/E3 defected-atoh1/EGFP were infused into the scala media through a hole made on the lateral wall of the cochlea. Six of the 12 animal were killed 2 weeks after the infusion operation. The others were killed 4 weeks after the operation. The whole mount of the basal membranes were directly observed under the fluorescence microscope for the expression of the EGFP (enhance green fluorescent protein) or for the expression of the hair cellspecific marker and nuclear after staining with myosin VIIa rabbit polyclonal antibody and Dapi dye. RESULT: New cells with big nuclear, ellipse body and expressed with EGFP were found in the region near to the outmost row of the outer hair cells in 2 animal 2 weeks after the infusion. Moreover there were 3 animals with specific morphologic new cells in the location where ever been located by the outer hair cells and the region as 2 weeks animals 4 weeks after the infusion. Those cells were stained by myosin VIIa antibody. CONCLUSION Atoh1 gene could transdifferent some supporting cells in the basal membrane into hair cell like cells in young adult guinea pigs in vivo. These supporting cells locate in the region of outer hair cells and the basal membrane which do not belong to the region of outer hair cells.
Animals ; Basic Helix-Loop-Helix Transcription Factors ; genetics ; metabolism ; Cell Transdifferentiation ; genetics ; Cochlea ; cytology ; Ear, Inner ; Green Fluorescent Proteins ; genetics ; metabolism ; Guinea Pigs ; Hair Cells, Auditory ; cytology ; Labyrinth Supporting Cells ; cytology

This article reported a case of nemaline myopathy caused by KLHL40 gene complex heterozygous mutations. This baby girl presented with shortness of breath, low myodynamia, and low muscle tension immediately after birth. However, her symptoms became worse after conventional treatment. Physical examination found lower muscle strength and muscle tone in four limbs and no primitive reflexes. The biochemistry test showed increased serum creatine kinase (CK). A muscle biopsy was not performed. The second-generation gene test confirmed the KLHL40 gene complex heterozygous mutations, which was a known mutation c.932G>T (p.R311L) and a de novo mutation c.1487T>A (p.M496K), inherited from the father and mother, respectively. Nemaline myopathy is a rare congenital muscular disease characterized by nemaline bodies in muscle fibers. Pathological and genetic diagnoses are the gold standards for the diagnosis of this disease.