ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

The professional identity and the influencing factors were surveyed among 110 resident physicians of general practice standardized training program in the First Affiliated Hospital of Xi'an Medical College with a self-designed questionnaire,and 100 valid questionnaires were received.The average score of professional identity was (66.10 ± 13.644),and the six dimensions ranked from high to low:professional behavior,professional efficacy,professional cognition,professional emotion,professional value and professional commitment.There were significant differences in the scores of professional identity among general practitioners with different monthly income(F=2.947,P=0.037).The survey indicates that the professional identity of the resident physicians of general practice standardized training program is generally low and the income is an important influencing factor.

Objective: To investigate the clinical research of Guo's Liulian therapy in treating acute pancreatitis intestinal mucosal barrier dysfunction and provide reference for the patients with acute pancreatitis. Methods: The 68 patients with acute pancreatitis who were admitted to our hospital from September 2016 to May 2018 were selected as study subjects. According to the random number table method, the patients were divided into the observation group and the control group, with 34 cases in each group. The patients in the control group were treated with conventional western medicine. The patients in the observation group were treated with Guo's Liulian therapy on the basis of the above treatment. The time of intestinal paralysis was compared between the two groups. The changes of intestinal mucosal barrier function and serum inflammatory factor related indexes before and after treatment were analyzed in the two groups. The difference of therapeutic effects between the two groups was observed. Results: In the observation group, the abdominal pain relief time, abdominal distention relief time, bowel sound recovery time, and first bowel anus defecation time were significantly lower than those in the control group (t=7.621, 5.332 6.625, 8.762, all Ps<0.01). After treatment, serum LPS, DAO, ET, D-lactic acid, TNF-α, IL-1, IL-6, IL-8, and IL-10 and urine L/M were significantly lower in the observation group, while the serum ITF and MFG-E8 were significantly higher in the observation group (t=9.856, 6.974, 9.784, 16.068, 9.550, 12.506, 22.343, 16.625, 6.774, 23.469, 20.118, 23.031, all Ps<0.01). Conclusions The Guo's Liulian therapy treatment of acute pancreatitis in patients with intestinal mucosal barrier dysfunction can reduce the palsy remission time, reduce inflammation, increase serum ITF, MFG-E8 levels, repair of intestinal permeability, and improve the intestinal barrier function.

OBJECTIVE: To explore the influence of hypoxemia on the hearing of children with childhood obstructive sleep apnea-hypopnea syndrome (OSAHS). METHOD: Auditory brainstem response (ABR) and distortion-product otoacoustic emission (DPOAE) was recorded in 68 ears and 60 ears respectively of children suffering from OSAHS with "A" tympanogram. Meanwhile, ABR and DPOAE was also recorded in 30 controls of children with "A" tympanogram. RESULT: There was no statistical difference between the mild OSAHS group and the control group in the latency of wave I, III and V, the interval between wave I and III, III and V, I and V. There was significant difference between the moderate and severe OSAHS group and the control group in the delayed latency of wave I. There was significant difference between the mild OSAHS group and the control group in the amplitudes of DPOAE at 8 kHz. There was significant difference between the moderate and severe OSAHS group and the control group in the amplitudes of DPOAE at 6 kHz and 8 kHz. CONCLUSION Cochlear function was affected when AHI > or = 10/h. ABR and DPOAE could be used to detect the early damagement of auditory function in childhood OSAHS.
Adolescent ; Child ; Child, Preschool ; Evoked Potentials, Auditory, Brain Stem ; Female ; Humans ; Male ; Otoacoustic Emissions, Spontaneous ; Sleep Apnea, Obstructive ; physiopathology

0.05).The blood loss in harmonic scalpel group was less than that in titanium clamp group or conventional group(P=0.001).CONCLUSION Harmonic scalpel is a new type of surgical instrument and is suitable for endoscopic thyroid surgery.It is worth of recommending that harmonic scalpel can not only increase safety of surgery and reduce blood loss,but also decrease the difficulty of operation and shorten the operation time.