Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

This study using maltodextrin as raw material, 1%-5% polyvinylpyrrolidone K30 as template agent, 1%-5% ammonium bicarbonate as pore-forming agent, curcumin and ibuprofen as model drugs. Porous maltodextrin was prepared by template and pore-forming agent methods, respectively. The structure and drug delivery behavior of porous maltodextrin prepared by different technologies were comprehensively characterized. The results showed that the porous maltodextrin prepared by pore-forming agent method had larger specific surface area (6.449 4 m²·g^-1) and pore size (32.804 2 nm), which was significantly better than that by template agent method (3.670 2 m²·g^-1, 15.278 5 nm). The adsorption kinetics between porous maltodextrin prepared by pore-forming agent method and curcumin were suitable for quasi-first order adsorption kinetic model, and that between porous maltodextrin and ibuprofen were suitable for quasi-second order adsorption kinetic model. While the adsorption kinetics between porous maltodextrin prepared by template agent method and two model drugs were both suitable for the quasi-first order adsorption kinetic model. In addition, the dissolution behavior analysis showed that the porous maltodextrin prepared by the two technologies can significantly improve the dissolution behavior of insoluble drugs, and the drug release was both carried out by diffusion mechanism, which suitable for the Peppas kinetic release model, but the porous maltodextrin prepared by template agent method had a faster release rate. The change of nozzle diameter had no significant effect on the adsorption process and drug release behavior of porous maltodextrin. In conclusion, the porous maltodextrins prepared by two different technologies were both beneficial to the delivery of insoluble drugs, and the template agent method was the best for delivery of insoluble drugs. This study can provide theoretical basis for the preparation of porous particles, promote the application of porous particles in insoluble drugs, and improve the bioavailability of insoluble drugs.

Objective To analyze the epidemiological patterns and pathogens of clusters of diarrhea in Xicheng Distract , Beijing during 2017-2022 , in order to update the policy of prevention. Mehods Between January 2017 and December 2022, stool samples of patients and partly cooks in clusters of diarrhea were collected and tested by Real-time PCR for Rotavirus, Norovirus, Adenovirus, Sapovirus and Astrovirus. Part of ORF1/ORF2 from Norovirus positive samples were amplified using RT-PCR. PCR products were sequenced and the genetypes were determined. Results Four hundreds and one clusters of diarrheas were reported. Among them , 369 were reported in kindergartens, primary schools and secondary schools. The morbidities were 4.14, 2.13 and 0.69 per thousand, respectively. Seventy four cooks in 15 clusters of diarrhea were Norovirus positive. The rate was 8.67%. Among these pathogens, Norovirus had the largest proportion , but the trend was declining. At least three kinds of genetype of GⅡ Norovirus were detected every year. Conclusion Clusters of diarrhea mainly occurred in kindergartens, primary schools and secondary schools. Result from the increasing proportions of unknown-cause clusters of diarrhea, the testing methods and scopes of pathogens should be extended. Diverse genetypes of Norovirus coexist and alternate in Beijing. So appearance of new genetypes and recombination of existed ones of Norovirus should be closely concerned.

Objective To evaluate the efficacy and safety of brexpiprazole in treating acute schizophrenia.Methods Patients with schizophrenia were randomly divided into treatment group and control group.The treatment group was given brexpiprozole 2-4 mg·d-1 orally and the control group was given aripiprazole 10-20 mg·d-1orally,both were treated for 6 weeks.Clinical efficacy of the two groups,the response rate at endpoint,the changes from baseline to endpoint of Positive and Negative Syndrome Scale(PANSS),Clinical Global Impression-Improvement(CGI-S),Personal and Social Performance scale(PSP),PANSS Positive syndrome subscale,PANSS negative syndrome subscale were compared.The incidence of treatment-related adverse events in two groups were compared.Results There were 184 patients in treatment group and 186 patients in control group.After treatment,the response rates of treatment group and control group were 79.50％(140 cases/184 cases)and 82.40％(150 cases/186 cases),the scores of CGI-I of treatment group and control group were(2.00±1.20)and(1.90±1.01),with no significant difference(all P＞0.05).From baseline to Week 6,the mean change of PANSS total score wese(-30.70±16.96)points in treatment group and(-32.20±17.00)points in control group,with no significant difference(P＞0.05).The changes of CGI-S scores in treatment group and control group were(-2.00±1.27)and(-1.90±1.22)points,PSP scores were(18.80±14.77)and(19.20±14.55)points,PANSS positive syndrome scores were(-10.30±5.93)and(-10.80±5.81)points,PANSS negative syndrome scores were(-6.80±5.98)and(-7.30±5.15)points,with no significant difference(P＞0.05).There was no significant difference in the incidence of treatment-related adverse events between the two group(69.00％vs.64.50％,P＞0.05).Conclusion The non-inferiority of Brexpiprazole to aripiprazole was established,with comparable efficacy and acceptability.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

It is unclear whether forearm and crural muscle fibers extend distally across the wrist and ankle joints, respectively.We hypothesized, in late-term fetuses, an over-production of muscle bellies extending over the joint. Muscle fibers in histological sections from unilateral wrists and ankles of 16 late-term fetuses (30–40 weeks) were examined and compared with 15 adult cadavers. Muscle fibers of the flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS) in fetuses, especially muscle bellies to the third and fourth fingers, were found to extend far distally beyond the radiocarpal joint.The extensor digitorum and extensor pollicis longus on the extensor side of the wrist were found to carry distally-extending muscle fibers, but these fibers did not extend beyond the distal end of the radius. In the ankle, most muscle bundles in the flexor hallucis longus (FHL), fibularis brevis (FB) and extensor digitorum longus extended distally beyond the talocrural joint, with most FB muscle fibers reaching the level of the talocalcaneal joint. In adult cadavers, muscle fibers of the FDP and FHL did not reach the levels of the radiocarpal and talocrural joints, respectively, whereas the FB muscle belly always reached the talocalcaneal joint. Similarly, some of the FDS reached the level of the radiocarpal joint. Generally, infants’ movements at the wrist and ankle could result in friction injury to over-extended muscle. However, the calcaneal and FDP tendons might protect the FB and FDS tendons, respectively, from friction stress.

The human fetal sacroiliac joint (SIJ) is characterized by unequal development of the paired bones and delayed cavitation. Thus, during the long in utero period, the bony ilium becomes adjacent to the cartilaginous sacrum. This mor phology may be analogous to that of the temporomandibular joint (TMJ). We examined horizontal histological sections of 24 fetuses at 10–30 weeks and compared the timing and sequences of joint cartilage development, cavitation, and ossification of the ilium. We also examined histological sections of the TMJ and humeroradial joint, because these also contain a disk or disk-like structure. In the ilium, endochondral ossification started in the anterior side of the SIJ, extended posteriorly and reached the joint at 12 weeks GA, and then extended over the joint at 15 weeks GA. Likewise, the joint cartilage appeared at the anterior end of the future SIJ at 12 weeks GA, and extended along the bony ilium posteriorly to cover the entire SIJ at 26 weeks GA. The cavitation started at 15 weeks GA. Therefore, joint cartilage development seemed to follow the ossification of the ilium by extending along the SIJ, and cavitation then occurred. This sequence “ossification, followed by joint cartilage formation, and then cavitation” did not occur in the TMJ or humeroradial joint. The TMJ had a periosteum-like membrane that covered the joint surface, but the humeroradial joint did not. After muscle contraction starts, it is likely that the mechanical stress from the bony ilium induces development of joint cartilage.

Humans ; Adult ; Serum Albumin, Human ; Consensus ; Cardiac Surgical Procedures ; Thoracic Surgery