Excavating the Scientific Approach and Efficacy of Kavuli Kalam and Savvu Varmam in Treating Epilepsy

In recent days, Siddha system of medicine has emerged as an arena for research especially in varma. Nearly 14.5 lakhs estimated number of people are reported to be affected with epilepsy in India every year. Researchers have concluded that stimulation of kavuli kalam, savvu varmam has powerful effects on epilepsy. The primary objective of this review was to describe the scientific approach and efficacy of kavuli kalam and savvu varmam in treating epilepsy. To treat epilepsy, the electrical disturbances in nerve cell have to be regulated. Stimulation of kavuli kalam and savvu varmam has powerful effect on autonomic nervous system and thereby regulating the sympathetic and parasympathetic nervous activation which leads to balancing the abnormal electrical activity. The effect is also related to muscle, nervous system and blood supply. This review article critically explores the novelty behind the stimulation of kai kavuli kalam, nadu kavuli and savuu varmam for the effective management of epilepsy.

Predicting Alzheimer's Disease Progression by Combining Multiple Measures

Alzheimer's disease (AD) is a degenerative brain ailment that affects millions worldwide. It is the most common form of dementia. Patients with an early diagnosis of Alzheimer's disease have a strong chance of preventing additional brain damage by halting nerve cell death. At the same time, it begins to progress several years before any symptoms appear. The variety of data is the biggest problem encountered during diagnosis. Neurological examination, brain imaging, and often asked questions from his connected closed relatives are the three forms of data that a neurologist or geriatrics employs to diagnose patients. One of the biggest questions which need answering is the choice of a convenient feature. The main objective of this paper is to help neurologists or geriatricians diagnose patient conditions. It proposes a new hybrid model for features extracted from medical data. It discusses AD's early diagnosis and progression for all features considered in the diagnosis and their complex interactions. It proves to have the best accuracy when compared with the state-ofthe-art algorithm. Also, it proves to be more accurate against some recent research ideas. It got 95% in all cases, considering this work focused more on increasing the number of instances in comparison.

Lipoic acid inhibits nerve cell apoptosis in rats with Parkinson's disease via Erk signaling pathway

Purpose: To investigate the effect of lipoic acid on nerve cell apoptosis in rats with Parkinson's disease via the extracellular signal-regulated kinase (ERK) signaling pathway.Methods: A total of 36 rats were randomly divided into normal group (n = 12), Parkinson's disease model group (n = 12) and lipoic acid group (n = 12). The neuronal morphology was examined by means of Nissl staining, while cell apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.Results: The neurons were severely damaged in model group, while neuronal morphology and structure were ameliorated in lipoic acid group when compared with those in model group. The p-ERK was lowered significantly (p < 0.05) in model group and lipoic acid group compared with that in normal group. Levels of mRNA, caspase-3 and Bax increased significantly, while Bcl-2 decreased in model group and lipoic acid group when compared with those in normal group (p < 0.05). Lipoic acid treatment significantly reduced mRNA expression of caspase-3 and Bax, but increased Bcl-2 compared with model group. Furthermore, ELISA results indicate that model and lipoic acid groups exhibited raised caspase-3 and Bax but significantly reduced Bcl-2 levels, compared with normal group. The results also showed that the apoptosis was higher in the other two groups than in normal group; on the other hand, it was significantly lower in lipoic acid group than in model group (p < 0.05).Conclusion: Lipoic acid inhibits nerve cell apoptosis in rats with Parkinson's disease by up-regulating ERK signaling pathway. Therefore, lipoic acid is a potential neuroprotective agent for the management of Parkinson’s disease.

Engineered extracellular vesicles derived from primary M2 macrophages with anti-inflammatory and neuroprotective properties for the treatment of spinal cord injury

Background Uncontrollable inflammation and nerve cell apoptosis are the most destructive pathological response after spinal cord injury (SCI). So, inflammation suppression combined with neuroprotection is one of the most promising strategies to treat SCI. Engineered extracellular vesicles with anti-inflammatory and neuroprotective properties are promising candidates for implementing these strategies for the treatment of SCI. Results By combining nerve growth factor (NGF) and curcumin (Cur), we prepared stable engineered extracellular vesicles of approximately 120 nm from primary M2 macrophages with anti-inflammatory and neuroprotective properties (Cur@EVs−cl−NGF). Notably, NGF was coupled with EVs by matrix metalloproteinase 9 (MMP9)-a cleavable linker to release at the injured site accurately. Through targeted experiments, we found that these extracellular vesicles could actively and effectively accumulate at the injured site of SCI mice, which greatly improved the bioavailability of the drugs. Subsequently, Cur@EVs−cl−NGF reached the injured site and could effectively inhibit the uncontrollable inflammatory response to protect the spinal cord from secondary damage; in addition, Cur@EVs−cl−NGF could release NGF into the microenvironment in time to exert a neuroprotective effect against nerve cell damage. Conclusions A series of in vivo and in vitro experiments showed that the engineered extracellular vesicles significantly improved the microenvironment after injury and promoted the recovery of motor function after SCI. We provide a new method for inflammation suppression combined with neuroprotective strategies to treat SCI. Graphical Abstract

Expression of p16 Within Myenteric Neurons of the Aged Colon: A Potential Marker of Declining Function

Human colonic neuromuscular functions decline among the elderly. The aim was to explore the involvement of senescence. A preliminary PCR study looked for age-dependent differences in expression of CDKN1A (encoding the senescence-related p21 protein) and CDKN2A (encoding p16 and p14) in human ascending and descending colon (without mucosa) from 39 (approximately 50: 50 male: female) adult (aged 27–60 years) and elderly donors (70–89 years). Other genes from different aging pathways (e.g., inflammation, oxidative stress, autophagy) and cell-types (e.g., neurons, neuron axonal transport) were also examined. Unlike CDKN1A, CDKN2A (using primers for p16 and p14 but not when using p14-specific primers) was upregulated in both regions of colon. Compared with the number of genes appearing to upregulate in association with temporal age, more genes positively associated with increased CDKN2A expression (respectively, 16 and five of 44 genes studied for ascending and descending colon). Confirmation of increased expression of CDKN2A was sought by immunostaining for p16 in the myenteric plexus of colon from 52 patients, using a semi-automated software protocol. The results showed increased staining not within the glial cells (S100 stained), but in the cytoplasm of myenteric nerve cell bodies (MAP2 stained, with identified nucleus) of ascending, but not descending colon of the elderly, and not in the cell nucleus of either region or age group (5,710 neurons analyzed: n = 12–14 for each group). It was concluded that increased p16 staining within the cytoplasm of myenteric nerve cell bodies of elderly ascending (but not descending) colon, suggests a region-dependent, post-mitotic cellular senescence-like activity, perhaps involved with aging of enteric neurons within the colon.

Bone Marrow Mesenchymal Stem Cells (BMSCs) Promote Neuronal Cell Repair in Spinal Cord Injury by Regulating Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

SCI (SCI) poses a challenge to nerve cell repair strategies. SCI injury can lead to the development of inflammation, which in turn can exacerbate nerve cell damage. The TLR4/NF-kappa B signaling pathway is a common inflammatory signaling pathway. Since BMSCs are involved in injury repair, whether they can promote the repair of SCI neuronal cells have not been reported. Spinal cord nerve cells were cultured in vitro and divided into mechanical injury group and BMSCs group followed by analysis of cell proliferation activity and detection of altered apoptotic activity. Changes in the concentrations of IL-6 and IL-1β were measured by ELISA and cellular mitochondrial alterations was assessed by JG-B staining along with analysis of NF-kappa B, TLR4, related neurodevelopmental factor BDNF, and NGF expression by western blot. Mechanical damage to neuronal cells resulted in decreased cell proliferation, increased apoptotic activity, decreased cellular mitochondrial activity, increased TLR4 and NF-kappa B expression, decreased BDNF and NGF expression, as well as increased secertions of IL-6 and IL-1β (P < 0.05). In contrast, co-culture with BMSCs resulted in increased proliferation and decreased apoptosis of mechanically injured neuronal cells, increased cellular mitochondrial activity, with observation of the inverse changes in other factors (P < 0.05). In conclusion, BMSCs can suppress inflammation and promote repair of injured neuronal cells by inhibiting TLR4/NF-kappa B signaling.

Morphological Signs of Dystrophy, Regeneration and Hypertrophy of Neurons

Results: Dystrophic changes constitute an extensive group of neuronal disorders and are manifested at the morphological level by deformation of the perikarions and neuropil, wrinkling or swelling of the cell, and changes in the chromatophilia of the cytoplasm. At the electron microscopic level, disorganization of organelles is observed, reflecting gross violations of the vital processes of the neuron. There are several ways to regenerate neurons: intracellular regeneration, restoration of the neuropil, the formation of new neurons (in some parts of the nervous system - the hippocampus, the subventricular layer of the lateral ventricles and olfactory bulbs) and the formation of heterokaryons (fusion of a neuron with an oligodendrocyte). Hypertrophy of neurons may indicate both compensation and the development of a pathological process. To clarify the nature of this phenomenon, it is necessary to conduct an ultramicroscopic study of the organelles of the nerve cell.

Clinical Significance of Changes in the Subendocortical Volume of Wilson Disease

Wilson disease (WD) is a rare neurogenetic disease with a variety of clinical manifestations. The disorder of copper metabolism can lead to cell necrosis, while nerve cell necrosis can reduce the volume of the corresponding parts. This study quantifies the degree of nerve cell injury by studying the subcortical volume changes in WD patients, and discusses the correlation between nerve cell injury in different parts and clinical manifestations. The results showed that compared with the healthy control group, the subcortical volume of WD decreased significantly, and the decrease in different parts was related to clinical symptoms. This study shows that we can quantify the degree of nerve cell injury by measuring the change of subcortical volume. Predict possible clinical symptoms.