scholarly journals Long-term ustekinumab treatment for refractory type I pityriasis rubra pilaris

Author(s):  
Alessandro Di Stefani ◽  
Marco Galluzzo ◽  
Marina Talamonti ◽  
Andrea Chiricozzi ◽  
Antonio Costanzo ◽  
...  
2018 ◽  
Vol 4 (4) ◽  
pp. 519-522
Author(s):  
Jeyakumar S ◽  
Jagatheesan Alagesan ◽  
T.S. Muthukumar

Background: Frozen shoulder is disorder of the connective tissue that limits the normal Range of motion of the shoulder in diabetes, frozen shoulder is thought to be caused by changes to the collagen in the shoulder joint as a result of long term Hypoglycemia. Mobilization is a therapeutic movement of the joint. The goal is to restore normal joint motion and rhythm. The use of mobilization with movement for peripheral joints was developed by mulligan. This technique combines a sustained application of manual technique “gliding” force to the joint with concurrent physiologic motion of joint, either actively or passively. This study aims to find out the effects of mobilization with movement and end range mobilization in frozen shoulder in Type I diabetics. Materials and Methods: 30 subjects both male and female, suffering with shoulder pain and clinically diagnosed with frozen shoulder was recruited for the study and divided into two groups with 15 patients each based on convenient sampling method. Group A patients received mobilization with movement and Group B patients received end range mobilization for three weeks. The outcome measurements were SPADI, Functional hand to back scale, abduction range of motion using goniometer and VAS. Results: The mean values of all parameters showed significant differences in group A as compared to group B in terms of decreased pain, increased abduction range and other outcome measures. Conclusion: Based on the results it has been concluded that treating the type 1 diabetic patient with frozen shoulder, mobilization with movement exercise shows better results than end range mobilization in reducing pain and increase functional activities and mobility in frozen shoulder.


Diabetes ◽  
1984 ◽  
Vol 33 (4) ◽  
pp. 394-400 ◽  
Author(s):  
G. Bolli ◽  
P. De Feo ◽  
S. De Cosmo ◽  
G. Perriello ◽  
G. Angeletti ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Inah Hwang ◽  
Hiroki Uchida ◽  
Ziwei Dai ◽  
Fei Li ◽  
Teresa Sanchez ◽  
...  

AbstractNeural stem/progenitor cells (NSPCs) persist over the lifespan while encountering constant challenges from age or injury related brain environmental changes like elevated oxidative stress. But how oxidative stress regulates NSPC and its neurogenic differentiation is less clear. Here we report that acutely elevated cellular oxidative stress in NSPCs modulates neurogenic differentiation through induction of Forkhead box protein O3 (FOXO3)-mediated cGAS/STING and type I interferon (IFN-I) responses. We show that oxidative stress activates FOXO3 and its transcriptional target glycine-N-methyltransferase (GNMT) whose upregulation triggers depletion of s-adenosylmethionine (SAM), a key co-substrate involved in methyl group transfer reactions. Mechanistically, we demonstrate that reduced intracellular SAM availability disrupts carboxymethylation and maturation of nuclear lamin, which induce cytosolic release of chromatin fragments and subsequent activation of the cGAS/STING-IFN-I cascade to suppress neurogenic differentiation. Together, our findings suggest the FOXO3-GNMT/SAM-lamin-cGAS/STING-IFN-I signaling cascade as a critical stress response program that regulates long-term regenerative potential.


Author(s):  
Rafique Umer Harvitkar ◽  
Abhijit Joshi

Abstract Introduction Laparoscopic fundoplication (LF) has almost completely replaced the open procedure performed for gastroesophageal reflux disease (GERD) and hiatus hernia (HH). Several studies have suggested that long-term results with surgery for GERD are better than a medical line of management. In this retrospective study, we outline our experience with LF over 10 years. Also, we analyze the factors that would help us in better patient selection, thereby positively affecting the outcomes of surgery. Patients and Methods In this retrospective study, we identified 27 patients (14 females and 13 males) operated upon by a single surgeon from 2010 to 2020 at our institution. Out of these, 25 patients (12 females and 13 males) had GERD with type I HH and 2 (both females) had type II HH without GERD. The age range was 24 to 75 years. All patients had undergone oesophago-gastro-duodenoscopy (OGD scopy). A total of 25 patients had various degrees of esophagitis. Two patients had no esophagitis. These patients were analyzed for age, sex, symptoms, preoperative evaluation, exact procedure performed (Nissen’s vs. Toupet’s vs. cruroplasty + gastropexy), morbidity/mortality, and functional outcomes. They were also reviewed to examine the length of stay, length of procedure, complications, and recurrent symptoms on follow-up. Symptoms were assessed objectively with a score for six classical GERD symptoms preoperatively and on follow-up at 1-, 4- and 6-weeks postsurgery. Further evaluation was performed after 6 months and then annually for 2 years. Results 14 females (53%) and 13 males (48%) with a diagnosis of GERD (with type I HH) and type II HH were operated upon. The mean age was 46 years (24–75 years) and the mean body mass index (BMI) was 27 (18–32). The range of duration of the preoperative symptoms was 6 months to 2 years. The average operating time dropped from 130 minutes for the first 12 cases to 90 minutes for the last 15 cases. The mean hospital stay was 3 days (range: 2–4 days). In the immediate postoperative period, 72% (n = 18) of the patients reported improvement in the GERD symptoms, while 2 (8%) patients described heartburn (grade I, mild, daily) and 1 (4%) patient described bloating (grade I, daily). A total of 5 patients (20%) reported mild dysphagia to solids in the first 2 postoperative weeks. These symptoms settled down after 2 to 5 weeks of postoperative proton-pump inhibitor (PPI) therapy and by adjusting consistency of oral feeds. There was no conversion to open, and we observed no perioperative mortality. There were no patients who underwent redo surgeries in the series. Conclusion LF is a safe and highly effective procedure for a patient with symptoms of GERD, and it gives long-term relief from the symptoms. Stringent selection criteria are necessary to optimize the results of surgery. Experience is associated with a significant reduction of operating time.


2010 ◽  
Vol 25 (9) ◽  
pp. 2976-2981 ◽  
Author(s):  
E. Puricelli ◽  
A. Bettinelli ◽  
N. Borsa ◽  
F. Sironi ◽  
C. Mattiello ◽  
...  

Neurosurgery ◽  
2017 ◽  
Vol 81 (1) ◽  
pp. 29-44 ◽  
Author(s):  
Jörg Klekamp

Abstract BACKGROUND: The clinical significance of pathologies of the spinal dura is often unclear and their management controversial. OBJECTIVE: To classify spinal dural pathologies analogous to vascular aneurysms, present their symptoms and surgical results. METHODS: Among 1519 patients with spinal space-occupying lesions, 66 patients demonstrated dural pathologies. Neuroradiological and surgical features were reviewed and clinical data analyzed. RESULTS: Saccular dural diverticula (type I, n = 28) caused by defects of both dural layers, dissections between dural layers (type II, n = 29) due to defects of the inner layer, and dural ectasias (type III, n = 9) related to structural changes of the dura were distinguished. For all types, symptoms consisted of local pain followed by signs of radiculopathy or myelopathy, while one patient with dural ectasia presented a low-pressure syndrome and 10 patients with dural dissections additional spinal cord herniation. Type I and type II pathologies required occlusion of their dural defects via extradural (type I) or intradural (type II) approaches. For type III pathologies of the dural sac no surgery was recommended. Favorable results were obtained in all 14 patients with type I and 13 of 15 patients with type II pathologies undergoing surgery. CONCLUSION: The majority of dural pathologies involving root sleeves remain asymptomatic, while those of the dural sac commonly lead to pain and neurological symptoms. Type I and type II pathologies were treated with good long-term results occluding their dural defects, while ectasias of the dural sac (type III) were managed conservatively.


Author(s):  
G. Licata ◽  
A. Gambardella ◽  
G. Calabrese ◽  
F. Pagliuca ◽  
R. Alfano ◽  
...  

2013 ◽  
Vol 19 (16) ◽  
pp. 4404-4411 ◽  
Author(s):  
Jessica J. O'Konek ◽  
Shingo Kato ◽  
Satomi Takao ◽  
Liat Izhak ◽  
Zheng Xia ◽  
...  

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 82
Author(s):  
Isabela A. Finamor ◽  
Caroline A. Bressan ◽  
Isabel Torres-Cuevas ◽  
Sergio Rius-Pérez ◽  
Marcelo da Veiga ◽  
...  

Background: Aspartame is an artificial sweetener used in foods and beverages worldwide. However, it is linked to oxidative stress, inflammation, and liver damage through mechanisms that are not fully elucidated yet. This work aimed to investigate the effects of long-term administration of aspartame on the oxidative and inflammatory mechanisms associated with liver fibrosis progression in mice. Methods: Mice were divided into two groups with six animals each: control and aspartame. Aspartame (80 mg/kg, via oral) or vehicle was administrated for 12 weeks. Results: Aspartame caused liver damage and elevated serum transaminase levels. Aspartame also generated liver fibrosis, as evidenced by histology analysis, and pro-fibrotic markers’ upregulation, including transforming growth factor β 1, collagen type I alpha 1, and alpha-smooth muscle actin. Furthermore, aspartame reduced nuclear factor erythroid 2-related factor 2 (Nrf2) activation and enzymatic antioxidant activity and increased lipid peroxidation, which triggered NOD-like receptor containing protein 3 (NLRP3) inflammasome activation and p53 induction. Furthermore, aspartame reduced peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) levels, possibly through p53 activation. This PGC-1α deficiency could be responsible for the changes in lipid profile in serum, total lipid accumulation, and gluconeogenesis impairment in liver, evidenced by the gluconeogenic enzymes’ downregulation, thus causing hypoglycemia. Conclusions: This work provides new insights to understand the mechanisms related to the adverse effects of aspartame on liver tissue.


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