CLINICAL STUDY OF GUGGULU GOLD AND GUM SHALLAKI ALONG WITH PANCHKARMA THERAPIES IN THE MANAGEMENT OF SANDHIGHATA VATA W.S.R OSTEOARTHRITIS

In Vriddhavastha, most of the Dhatus Kshaya, which in turn leads to Vataprakopa and thus making individuals prone to many diseases. Among these diseases, Sandhigata Vata is one type of Vata-Vyadhi, which is the commonest form and occurs mainly due to sitting jobs, air conditioner atmosphere, lack of proper healthy diet, travelling and old age etc. Sandhigata Vata is one of the most common Vatavyadhi, which can be correlated with osteoarthritis. The prevalence rate of Osteoarthritis is about 14.8 %, in which knee osteoarthritis prevalence rate is 10.8% which is more than the arthritis of other joints1. The incidence of osteoarthritis in India is as high as 12%. It is estimated that approximately four out of 100 people are affected by it. Osteoarthritis is the most common articular disorder which begins asymptomatically in the 2nd & 3rd decades and is extremely common by age 70. Almost all persons by age 40 have some pathologic change in the weight-bearing joint. 25% of females & 16% of males have symptomatic osteoarthritis. When we talk about healthy joints, there is a coating of tough but smooth and slippery tissue, called cartilage, which covers the surface of the bones and helps the bones to move freely against each other. When a joint develops osteoarthritis, part of the cartilage thins and the surface becomes rougher, which in turn doesn't allow the joint to move as smoothly as it should. When cartilage becomes damaged, all the tissues within the joint become more active than normal as the body tries to repair itself. But these repair processes are going to change not only the structure of the joint but will often allow the joint to work normally and without any pain and stiffness. Acharya Charaka has mentioned "Sandhi Gataanila”, which means vata gets located in the Sandhi and thereafter results in Sandhigatavata. Allopathic treatment has its limitation in managing this disease. It can provide either conservative or surgical treatment and can only subside the pain but not cure the cause of diseases. While traditional life science Ayurveda has the most effective solution over this. Local Abhyanga and Nadi Sweda were selected for the present study in one group, as it has shown best for the Vata Vyadhis. Here local Abhyanga was given with Bala Taila because Bala Taila and Nadi Sweda are having Vatashamaka and Rasayana properties. While in the case of another group, Guggulu gold along with gum shallaki followed by local Abhyanga and Nadi Sweda were given to the patients. Keywords: Vridhavastha, Dhatus Kshaya, Sandhigata Vata Abhyanga, Vatashamaka, Rasayana, Guggulu gold, Gum Shallaki, Nadi Sweda

Single-synapse analyses of Alzheimers disease implicate pathologic tau, DJ1, CD47, and ApoE

Synaptic molecular characterization is limited for Alzheimers disease (AD). We used mass cytometry to quantify 38 probes in approximately 17 million single synaptic events from human brains without pathologic change or with pure AD or Lewy body disease (LBD), non-human primates (NHP), and PS/APP mice. Synaptic molecular integrity in humans and NHP was similar. Although not detected in human synapses, Aβ was in PS/APP mice synaptic events. Clustering and pattern identification of human synapses showed expected disease-specific differences, like increased hippocampal pathologic tau in AD and reduced caudate dopamine transporter in LBD, and revealed novel findings including increased hippocampal CD47 and lowered DJ1 in AD and higher ApoE in AD dementia. Our results were independently supported by multiplex ion beam imaging of intact tissue.

The formation mechanism of acute dissection of blood blister-like aneurysm and its implication of endovascular treatment

Background Acute mural dissection of the anterior wall of the internal carotid artery which may contribute to the development of blood blister-like aneurysms (BBLAs) was postulated, and stenting or flow diversion treatment across the soi-disant aneurysm was reported in this study. Methods From December 2016 to December 2018, 8 patients presenting with subarachnoid hemorrhage (SAH) due to BBLA were subjected to endovascular treatment with stent-assisted coiling. Clinical outcomes were evaluated using a clinical outcome score scale. Results Based on angiograms, pathologic change involving the supraclinoid segments of the internal carotid artery (ICA) adjacent to BBLA was found in all patients. This pathologic change meant a focal dissection of the supraclinoid segment of the ICA which constituted the pathogenesis of BBLAs. Closed-cell, open-cell, and braided stents were used in 1, 1, and 6 patients, respectively. Complete obliteration was achieved following endovascular treatment among all 8 patients harboring BBLA. One re-bleeding successive to a closed-cell stent across the aneurysmal neck was observed. Follow-up angiograms revealed stable complete exclusion of all BBLAs from the parent vessel at 3 to 8 months. All patients had a favorable clinical outcome score of 0–1. Conclusions Acute dissection of a focal point of the intracranial vessels underlies the development of BBLAs. Open-cell and braided-cell stent-assisted coiling may constitute appropriate treatment due to good apposition against the vascular walls. Adjunctive coils may facilitate immediate complete occlusion of BBLAs.

In Vivo Amyloid, Neurodegeneration, and Verbal Learning in Late Middle-Aged Hispanics

Background: The National Institute on Aging (NIA)/Alzheimer’s Association (AA) 2018 framework conceptualizes Alzheimer’s disease (AD) biologically. Evidence of brain amyloid by biomarkers defines AD pathologic change and the Alzheimer’s continuum. The presence of tau or neurodegeneration in the absence of amyloid defines non-AD pathologic change. Objective: To examine the relation of in vivo amyloid and neurodegeneration with verbal learning, one of the cognitive abilities affected early in AD, in late middle age. Methods: This was a cross-sectional study of amyloid and neurodegeneration biomarkers in a community-based cohort of 350 late-middle aged Hispanics without dementia (mean age: 64.15±3.34; 72.0%women). Amyloid (A) was measured as global standardized uptake value ratio (SUVR) with 18F-Florbetaben positron emission tomography (PET). Neurodegeneration (N) was ascertained as cortical thickness (CT) in AD signature areas using brain magnetic resonance imaging. We examined A/N continuously, categorically, by A/N profiles, and profile categories. The amyloid threshold for positivity was defined using the K means method. The CT threshold was defined as 2 standard deviations below the mean CT. Verbal learning was ascertained using total recall and delayed recall in the Buschke Selective Reminding test (SRT). Results: Higher cortical thickness was associated with higher performance in SRT delayed recall. Amyloid SUVR was not related to SRT performance. The low CT category was associated with lower performance in SRT delayed recall, while Amyloid categories were not related to any SRT score. The non-AD pathologic change group (A-N+) performed worse in SRT delayed recall compared to the Normal A/N profile group (A-N-). Conclusion: In late middle-aged Hispanics without dementia, non-AD pathologic change, but not the Alzheimer’s continuum, was related to verbal learning.

Squamous metaplasia of the rete ovarii do not suppress ovarian cyclicity and pregnancy in cattle: case report

ABSTRACT Squamous metaplasia of the rete ovarii is an ovarian pathologic change characterized by replacement of the normal single layered cuboidal epithelium of the rete ovarii by a stratified squamous keratinized epithelium. Uterus and ovaries from a local slaughterhouse pregnant crossbreed cow were evaluated through ultrasound, macroscopically and histologically. Grossly, there were multiple cysts in both ovaries, which were histologically characterized as rete ovarii cysts with squamous metaplasia and intraluminal accumulation of keratinized material. Squamous metaplasia of the rete ovarii has been previously reported in cows, however this is the first report of this condition in a pregnant animal, demonstrating that this ovarian change is compatible with pregnancy.

Clinician-judged hearing impairment and associations with neuropathologic burden

ObjectiveTo examine whether neuropathologic burden is associated with hearing impairment.MethodsWe studied 2,755 autopsied participants ≥55 years of age from the National Alzheimer's Coordinating Center database. Participants had at least 1 clinical evaluation at US National Institute on Aging–funded Alzheimer's Disease Center no more than 2 years before death. Patients were classified as hearing impaired by clinician report at baseline. Common dementia neuropathologies included Alzheimer disease pathologic change (Consortium to Establish a Registry for Alzheimer's Disease neuritic plaque density, neurofibrillary degeneration Braak stage), Lewy body disease, gross infarcts, and microinfarcts. Logistic regression models predicted impaired hearing with adjustment for age at death, sex, race, education, center, and follow-up time. Relative risks were calculated with the use of marginal standardization.ResultsImpaired hearing was common (32%). In participants who were cognitively normal at baseline (n = 580), impaired hearing was associated with higher Braak stage (relative risk [RR] 1.33 per 2-stage increase, 95% confidence interval [CI] 1.06–1.66) but not other pathologies. In participants with dementia (n = 2,175), impaired hearing was positively associated with microinfarcts (RR 1.18, 95% CI 1.00–1.39) and inversely associated with neuritic plaque density (RR 0.91 per score increase, 95% CI 0.85–0.99). Development of impaired hearing in those with cognitive impairment was associated with neocortical Lewy bodies (1.26, 95% CI 1.02–1.55).ConclusionsImpaired hearing, reported before the onset of cognitive impairment, was associated with increased neurofibrillary tangle burden. Impaired hearing in those with cognitive impairment was associated with microinfarcts and neocortical Lewy bodies but not typical Alzheimer disease pathologic change. Functional hearing problems may be a preclinical marker of neurofibrillary neurodegeneration, although replication is needed.

Relationship between β-amyloid and structural network topology in decedents without dementia

ObjectiveTo investigate the association between β-amyloid (Aβ) load and postmortem structural network topology in decedents without dementia.MethodsFourteen decedents (mean age at death 72.6 ± 7.2 years) without known clinical diagnosis of neurodegenerative disease and meeting pathology criteria only for no or low Alzheimer disease (AD) pathologic change were selected from the Normal Aging Brain Collection Amsterdam database. In situ brain MRI included 3D T1-weighted images for anatomical registration and diffusion tensor imaging for probabilistic tractography with subsequent structural network construction. Network topologic measures of centrality (degree), integration (global efficiency), and segregation (clustering and local efficiency) were calculated. Tissue sections from 12 cortical regions were sampled and immunostained for Aβ and hyperphosphorylated tau (p-tau), and histopathologic burden was determined. Linear mixed effect models were used to assess the relationship between Aβ and p-tau load and network topologic measures.ResultsAβ was present in 79% of cases and predominantly consisted of diffuse plaques; p-tau was sparsely present. Linear mixed effect models showed independent negative associations between Aβ load and global efficiency (β = −0.83 × 10−3, p = 0.014), degree (β = −0.47, p = 0.034), and clustering (β = −0.55 × 10−2, p = 0.043). A positive association was present between Aβ load and local efficiency (β = 3.16 × 10−3, p = 0.035). Regionally, these results were significant in the posterior cingulate cortex (PCC) for degree (β = −2.22, p < 0.001) and local efficiency (β = 1.01 × 10−2, p = 0.014) and precuneus for clustering (β = −0.91 × 10−2, p = 0.017). There was no relationship between p-tau and network topology.ConclusionThis study in deceased adults with AD-related pathologic change provides evidence for a relationship among early Aβ accumulation, predominantly of the diffuse type, and structural network topology, specifically of the PCC and precuneus.

Electro-Acupuncture Accelerate Pressure Ulcer Healing by Increasing Asic3 Expression in Mouse Model

Background: The efficiency of insert electro-acupuncture stimulation (EAS) on improving pressure ulcer (PU) healing was still unclear. This study explored the effects of insert EAS on PU and provided the regulation information of acid-sensing ion channel 3 (Asic3) during EAS intervention.Methods: A total of 32 BALB/c mice were randomly divided into control group, model group, EAS group, ESA + APETx2 (Asic3 inhibitor) group, each for eight mice. The ulcer tissues of all mice were havest at 14 days after modeling. HE stains and mmunohistochemical staining evaluated the pathologic change, Western blot, and RT-PCR evaluated Asic3 expression. Results: Compared with the model group, EAS group showed alleviated epithelial thickness, increased number of fibroblasts, and reduced inflammatory cell infiltration. Thickened epithelium, decreased number of fibroblasts, and obvious inflammatory cell infiltration in the EAS+APETx2 group were no significant differences with the model group. Asic3 expression in PU tissues in the EAS group was elevated compared with the model group. In addition, Asic3 expression was decreased in EAS + APETx2 group than the EAS group. Conclusion: EAS can accelerate the PU healing process in mice, and EAS also could improve the expression of Asic3 in PU tissues.Trial-registration: Not applicaple.