Aim To study the change of blood pressure in 1079 workers for fifteen years and the effect of anti-hypertension drugs therapy. Methods We investigated the blood pressure of 1079 workers who were enrolled in six organizations in the year 1983 and 1998 respectively. Results During the 15 years: (1)Mean value of blood pressure: systolic blood pressure increased 22 mmHg in man and 16.9 mmHg in women; diastolic blood pressure increased 9 mmHg in man and 12.7 mmHg in women (P<0.05);(2)The incidence of hypertension increased by 25.03% in man and 28.28% in women;(3)The prevalence rate of hypertension is 27.9 percent in people with initially normal blood pressure (1.86%/y) and 72.6 percent in initially broder line hypertension (4.84%/y);(4)The control rate of hypertension is 2.9 percent;(5)The incidence of stroke is highly related to hypertension (P<0.001);(6)46.6 percent patients had a regular drug therapy, mainly reserpini complex(25.2%);(7)Drug therapy has no obviously effect of the control of hypertension and the incidence of stroke. Conclusion Both the mean value of BP and the incidence of hypertension were increased with age. The control rate of hypertension was low and the drug therapy shows little advantage. We should do mach more works to popularize the knowledge of the prevention of hypertension. Improve people's self-prevention. Regular cheek should be given to the hypertension patients.

OBJECTIVE: To explore the interaction between Tubulin beta 4B class IVb (TUBB4B) and Agtpbp1/cytosolic carboxypeptidase- like1 (CCP1) in mouse primary spermatocytes (GC-2 cells) and the role of TUBB4B in regulating the development of GC-2 cells. METHODS: Lentiviral vectors were used to infect GC-2 cells to construct TUBB4B knockdown and negative control (NC-KD) cells. The stable cell lines with TUBB4B overexpression (Tubb4b-OE) and the negative control (NC-OE) cells were screened using purinomycin. RT-qPCR and Western blotting were used to verify successful cell modeling and explore the relationship between TUBB4B and CCP1 expressions in GC-2 cells. The effects of TUBB4B silencing and overexpression on the proliferation and cell cycle of GC-2 cells were evaluated using CCK8 assay and flow cytometry. The signaling pathway proteins showing significant changes in response to TUBB4B silencing or overexpression were identified using Western blotting and immunofluorescence assay and then labeled for verification at the cellular level. RESULTS: Both TUBB4B silencing and overexpression in GC-2 cells caused consistent changes in the mRNA and protein expressions of CCP1 (P < 0.05). Similarly, TUBB4B expression also showed consistent changes at the mRNA and protein after CCP1 knockdown and restoration (P < 0.05). TUBB4B knockdown and overexpression had no significant effect on proliferation rate or cell cycle of GC-2 cells, but caused significant changes in the key proteins of the nuclear factor kappa-B (NF-κB) signaling pathway (p65 and p-p65) and the mitogen-activated protein kinase (MAPK) signaling pathway (ErK1/2 and p-Erk1/2) (P < 0.05); CCP1 knockdown induced significant changes in PolyE expression in GC-2 cells (P < 0.05). CONCLUSIONS TUBB4B and CCP1 interact via a mutual positive regulation mechanism in GC-2 cells. CCP-1 can deglutamize TUBB4B, and the latter is involved in the regulation of NF-κB and MAPK signaling pathways in primary spermatocytes.
Animals ; Male ; Mice ; GTP-Binding Proteins/metabolism* ; Mitogen-Activated Protein Kinases/metabolism* ; NF-kappa B/metabolism* ; RNA, Messenger ; Serine-Type D-Ala-D-Ala Carboxypeptidase/metabolism* ; Signal Transduction ; Spermatocytes ; Tubulin/genetics*